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April 8, 2013 | https://www.sciencedaily.com/releases/2013/04/130408142644.htm | Avian virus may be harmful to cancer cells | A study at the Virginia-Maryland Regional College of Veterinary Medicine has identified a chicken-killing virus as a promising treatment for prostate cancer in humans. | Researchers have discovered that a genetically engineered Newcastle disease virus, which harms chickens but not humans, kills prostate cancer cells of all kinds, including hormone-resistant cancer cells. The work of Dr. Elankumaran Subbiah, associate professor of virology in the Department of Biomedical Sciences and Pathobiology, along with Dr. Siba Samal, associate dean and chairman of the University of Maryland's Department of Veterinary Medicine, and Shobana Raghunath, a graduate student in Subbiah's laboratory, appears in the April 2013 issue of the"This potential treatment is available for immediate pre-clinical and clinical trials, but these are typically not done at the university level," Subbiah said. "We are looking for commercial entities that are interested in licensing the technology for human clinical trials and treatment. Newcastle disease virus has yet to be tested as a treatment for prostate cancer in patients."About one in six men will develop prostate cancer. Patients typically receive hormone treatments or chemotherapy, both of which have adverse side effects. Subbiah hopes that the development of new treatment methodologies will not only better fight prostate cancer, but also lessen the side effects commonly associated with hormone treatments and chemotherapy.Newcastle disease virus affects domestic and wild bird species, especially chickens, and is one of the most economically important viruses to the poultry industry. Although it can cause mild conjunctivitis and flu-like symptoms in humans who have been in close contact with infected birds, it does not pose a threat to human health.Scientists first documented the cancer-fighting properties of Newcastle disease virus in the 1950s, but it is only with recent advances in reverse genetics technology that they have turned to the genetically engineered virus as a possible treatment."We modified the virus so that it replicates only in the presence of an active prostate-specific antigen and, therefore, is highly specific to prostate cancer. We also tested its efficacy in a tumor model in vitro," Subbiah said. "The recombinant virus efficiently and specifically killed prostate cancer cells, while sparing normal human cells in the laboratory, but it would take time for this to move from the discovery phase to a treatment for prostate cancer patients."Earlier human clinical trials for other types of cancer with naturally occurring strains of Newcastle disease virus required several injections of the virus in large quantities for success. Subbiah believes that the recombinant virus would be able to eradicate prostate cancer in much lower doses. It would also seek out metastatic prostate cancer cells and remove them. Because it is cancer cell-type specific, "the recombinant virus will be extremely safe and can be injected intravenously or directly into the tumor," Subbiah added.Subbiah received a $113,000 concept award from the U.S. Department of Defense to develop his prostate cancer treatment under a Congressionally-directed medical research program. He is seeking additional foundation and corporate funds to take his research to the next level.The researchers have also received a National Institutes of Health exploratory grant to develop the cell type-specific Newcastle disease virus for several other types of cancer cells, including breast, pancreas, brain, prostate, and multiple myeloma. "Although the virus can potentially treat many different types of cancer, we are focusing on these five," Subbiah said. | Genetically Modified | 2,013 |
April 8, 2013 | https://www.sciencedaily.com/releases/2013/04/130408085043.htm | Bird flu mutation study offers vaccine clue | Scientists have described small genetic changes that enable the H5N1 bird flu virus to replicate more easily in the noses of mammals. | So far there have only been isolated cases of bird flu in humans, and no widespread transmission as the H5N1 virus can't replicate efficiently in the nose. The new study, using weakened viruses in the lab, supports the conclusions of controversial research published in 2012 which demonstrated that just a few genetic mutations could enable bird flu to spread between ferrets, which are used to model flu infection in humans.Researchers say the new findings could help to develop more effective vaccines against new strains of bird flu that can spread between humans."Knowing why bird flu struggles to replicate in the nose and understanding the genetic mutations that would enable it to happen are vital for monitoring viruses circulating in birds and preparing for an outbreak in humans," said Professor Wendy Barclay, from the Department of Medicine at Imperial College London, who led the study."The studies published last year pointed to a mechanism that restricts replication of H5N1 viruses in the nose. We've engineered a different mutation with the same effect into one of the virus proteins and achieved a similar outcome. This suggests that there is a common mechanism by which bird flu could evolve to spread between humans, but that a number of different specific mutations might mediate that."Bird flu only rarely infects humans because the human nose has different receptors to those of birds and is also more acidic. The Imperial team studied mutations in the gene for haemagglutinin, a protein on the surface of the virus that enables it to get into host cells. They carried out their experiments in a laboratory strain of flu with the same proteins on its surface as bird flu, but engineered so that it cannot cause serious illness.The research found that mutations in the H5 haemagglutinin enabled the protein to tolerate higher levels of acidity. Viruses with these mutations and others that enabled them to bind to different receptors were able to replicate more efficiently in ferrets and spread from one animal to another.The results have important implications for designing vaccines against potential pandemic strains of bird flu. Live attenuated flu vaccines (LAIV) might be used in a pandemic situation because it is possible to manufacture many more doses of this type of vaccine than of the killed virus vaccines used to protect against seasonal flu. LAIV are based on weakened viruses that don't cause illness, but they still have to replicate in order to elicit a strong immune response. Viruses with modified haemagglutinin proteins induced strong antibody responses in ferrets in this study, suggesting that vaccines with similar modifications might prove more effective than those tested previously."We can't predict how bird flu viruses will evolve in the wild, but the more we understand about the kinds of mutations that will enable them to transmit between humans, the better we can prepare for a possible pandemic," said Professor Barclay.The research was funded by the Medical Research Council and the Wellcome Trust and published in the | Genetically Modified | 2,013 |
April 2, 2013 | https://www.sciencedaily.com/releases/2013/04/130402124811.htm | Fast track to mouse modeling | What genes are responsible for the development of breast cancer? What are the brain cell mutations that lead to the onset of Alzheimer's? To find new therapies, scientists have to understand how diseases are triggered at cell level. Experiments on genetically modified mice are an indispensable part of basic medical research. Now a method has been found to help laboratories carry out their work with fewer test animals. | Scientists use genetically modified laboratory mice to investigate the underlying mechanisms of diseases. These "knockout" mice carry genes or gene regions that are thought to trigger diseases.For laboratories, the knockout technique requires a lot of time and effort. "Scientists start by engineering a genetic defect into embryonic stem cells," explains Prof. Wolfgang Wurst, who carries out research at Technische Universität München (TUM) and Helmholtz Zentrum München. "Then they implant the manipulated stem cells into a mouse embryo."After multiple steps, organisms are created which have both modified and unmodified cells. The mice have to be crossed several times until offspring are produced which carry the knockout characteristic in all of their body cells. Including all tests, it takes scientists between one and two years to produce a functioning mouse model.But now the team led by Prof. Wurst and Dr. Ralf Kühn have developed a new method, allowing them to complete the process in a much shorter time -- just a little over four months. They modified the genes directly in the fertilized mouse egg cells so that all the cells in the bodies of the offspring would have the same genetic defect. "By eliminating the time-consuming crossing stage, laboratories will be able to produce mouse models much quicker and with much fewer test animals," remarks Wurst.The team used TALEN enzymes(*) for its research experiments. These DNA tools have a dual function: One part recognizes and binds to a particular gene, while another cuts the DNA strand in situ. These ultra-precise DNA "scalpels" were developed just a few years ago."TALEN enzymes have a simple, modular structure," says Wurst. "This means that we can create a number of variants to cut through all genes in the genome and modify them for a specific purpose." The technique will allow scientists to knock out particular genes, introduce genetic defects within cells and repair genetic defects."We have used the TALEN process to implant mutations associated with human dementia in mouse germ cells. These animal models will help us understand the molecular mechanisms behind dementia. The advantage of the technique is that we will in principle be able to model all hereditary diseases in the test mice," adds Wurst.(*)TALEN: | Genetically Modified | 2,013 |
March 30, 2013 | https://www.sciencedaily.com/releases/2013/03/130330130838.htm | Multi-toxin biotech crops not silver bullets, scientists warn | The popular new strategy of planting genetically engineered crops that make two or more toxins to fend off insect pests rests on assumptions that don't always apply, UA researchers have discovered. Their study helps explain why one major pest is evolving resistance much faster than predicted and offers ideas for more sustainable pest control. | A strategy widely used to prevent pests from quickly adapting to crop-protecting toxins may fail in some cases unless better preventive actions are taken, suggests new research by University of Arizona entomologists published in theCorn and cotton have been genetically modified to produce pest-killing proteins from the bacterium Although Bt crops have helped to reduce insecticide sprays, boost crop yields and increase farmer profits, their benefits will be short-lived if pests adapt rapidly, said Bruce Tabashnik, a co-author of the study and head of the UA department of entomology. "Our goal is to understand how insects evolve resistance so we can develop and implement more sustainable, environmentally friendly pest management," he said. Tabashnik and Carrière are both members of the UA's BIO5 Institute.Bt crops were first grown widely in 1996, and several pests have already become resistant to plants that produce a single Bt toxin. To thwart further evolution of pest resistance to Bt crops, farmers have recently shifted to the "pyramid" strategy: each plant produces two or more toxins that kill the same pest. As reported in the study, the pyramid strategy has been adopted extensively, with two-toxin Bt cotton completely replacing one-toxin Bt cotton since 2011 in the U.S.Most scientists agree that two-toxin plants will be more durable than one-toxin plants. The extent of the advantage of the pyramid strategy, however, rests on assumptions that are not always met, the study reports. Using lab experiments, computer simulations and analysis of published experimental data, the new results help explain why one major pest has started to become resistant faster than anticipated."The pyramid strategy has been touted mostly on the basis of simulation models," said Carrière. "We tested the underlying assumptions of the models in lab experiments with a major pest of corn and cotton. The results provide empirical data that can help to improve the models and make the crops more durable."One critical assumption of the pyramid strategy is that the crops provide redundant killing, Carrière explained. "Redundant killing can be achieved by plants producing two toxins that act in different ways to kill the same pest," he said, "so, if an individual pest has resistance to one toxin, the other toxin will kill it."In the real world, things are a bit more complicated, Carrière's team found out. Thierry Brévault, a visiting scientist from France, led the lab experiments at the UA. His home institution, the "We obviously can't release resistant insects into the field, so we breed them in the lab and bring in the crop plants to do feeding experiments," Carrière said. For their experiments, the group collected cotton bollworm -- also known as corn earworm or As expected, the resistant caterpillars survived after munching on cotton plants producing only that toxin. The surprise came when Carrière's team put them on pyramided Bt cotton containing Cry2Ab in addition to Cry1Ac.If the assumption of redundant killing is correct, caterpillars resistant to the first toxin should survive on one-toxin plants, but not on two-toxin plants, because the second toxin should kill them, Carrière explained."But on the two-toxin plants, the caterpillars selected for resistance to one toxin survived significantly better than caterpillars from a susceptible strain."These findings show that the crucial assumption of redundant killing does not apply in this case and may also explain the reports indicating some field populations of cotton bollworm rapidly evolved resistance to both toxins.Moreover, the team's analysis of published data from eight species of pests reveals that some degree of cross-resistance between Cry1 and Cry2 toxins occurred in 19 of 21 experiments. Contradicting the concept of redundant killing, cross-resistance means that selection with one toxin increases resistance to the other toxin.According to the study's authors, even low levels of cross-resistance can reduce redundant killing and undermine the pyramid strategy. Carrière explained that this is especially problematic with cotton bollworm and some other pests that are not highly susceptible to Bt toxins to begin with.The team found violations of other assumptions required for optimal success of the pyramid strategy. In particular, inheritance of resistance to plants producing only Bt toxin Cry1Ac was dominant, which is expected to reduce the ability of refuges to delay resistance.Refuges consist of standard plants that do not make Bt toxins and thus allow survival of susceptible pests. Under ideal conditions, inheritance of resistance is not dominant and the susceptible pests emerging from refuges greatly outnumber the resistant pests. If so, the matings between two resistant pests needed to produce resistant offspring are unlikely. But if inheritance of resistance is dominant, as seen with cotton bollworm, matings between a resistant moth and a susceptible moth can produce resistant offspring, which hastens resistance.According to Tabashnik, overly optimistic assumptions have led the EPA to greatly reduce requirements for planting refuges to slow evolution of pest resistance to two-toxin Bt crops.The new results should come as a wakeup call to consider larger refuges to push resistance further into the future, Carrière pointed out. "Our simulations tell us that with 10 percent of acreage set aside for refuges, resistance evolves quite fast, but if you put 30 or 40 percent aside, you can substantially delay it.""Our main message is to be more cautious, especially with a pest like the cotton bollworm," Carrière said. "We need more empirical data to refine our simulation models, optimize our strategies and really know how much refuge area is required. Meanwhile, let's not assume that the pyramid strategy is a silver bullet." | Genetically Modified | 2,013 |
March 29, 2013 | https://www.sciencedaily.com/releases/2013/03/130329161247.htm | Researchers engineer plant cell walls to boost sugar yields for biofuels | When blessed with a resource in overwhelming abundance it's generally a good idea to make valuable use of that resource. Lignocellulosic biomass is the most abundant organic material on Earth. For thousands of years it has been used as animal feed, and for the past two centuries has been a staple of the paper industry. This abundant resource, however, could also supply the sugars needed to produce advanced biofuels that can supplement or replace fossil fuels, providing several key technical challenges are met. | One of these challenges is finding ways to more cost-effectively extract those sugars. Major steps towards achieving this breakthrough are being taken by researchers at the U.S. Department of Energy (DOE)'s Joint BioEnergy Institute (JBEI)."Through the tools of synthetic biology, we have engineered healthy plants whose lignocellulosic biomass can more easily be broken down into simple sugars for biofuels," says Dominique Loque, who directs the cell wall engineering program for JBEI's Feedstocks Division. "Working with the model plant, JBEI is a scientific partnership led by Lawrence Berkeley National Laboratory (Berkeley Lab) whose mission is to advance the development of next generation biofuels that can provide the nation with clean, green and renewable transportation energy that will create jobs and boost the economy. Loque and his research group have focused on reducing the natural recalcitrance of plant cell walls to give up their sugars. Unlike the simple starch-based sugars in corn and other grains, the complex polysaccharide sugars in plant cell walls are locked within a robust aromatic polymer called lignin. Setting these sugars free from their lignin cage has required the use of expensive and environmentally harsh chemicals at high temperatures, a process that helps drive production costs of advance biofuels prohibitively high."By embedding polysaccharide polymers and reducing their extractability and accessibility to hydrolytic enzymes, lignin is the major contributor to cell wall recalcitrance," Loque says. "Unfortunately, most efforts to reduce lignin content during plant development have resulted in severe biomass yield reduction and a loss of integrity in vessels, a key tissue responsible for water and nutrient distribution from roots to the above-ground organs."Lignin has also long posed problems for pulping and animal feed. To overcome the lignin problem, Loque and his colleagues rewired the regulation of lignin biosynthesis and created an artificial positive feedback loop (APFL) to enhance secondary cell wall biosynthesis in specific tissue. The idea was to reduce cell wall recalcitrance and boost polysaccharide content without impacting plant development."When we applied our APFL to Loque and his colleagues believe that the APFL strategy they used to enhance polysaccharide deposition in the fibers of their "We now know that we can significantly re-engineer plant cell walls as long as we maintain the integrity of vessels and other key tissues," Loque says.A paper describing this research in detail has been published in This research was supported by the DOE Office of Science. | Genetically Modified | 2,013 |
March 28, 2013 | https://www.sciencedaily.com/releases/2013/03/130328125331.htm | Mate choice in mice is heavily influenced by paternal cues, mouse study shows | Hybrid offspring of different house mice populations show a preference for mating with individuals from their father's original population. | Mate choice is a key factor in the evolution of new animal species. The choice of a specific mate can decisively influence the evolutionary development of a species. In mice, the attractiveness of a potential mate is conveyed by scent cues and ultrasonic vocalizations. Researchers from the Max Planck Institute for Evolutionary Biology in Plön investigated whether house mice (Mus musculus) would mate with each other even if they were from two populations which had been separated from each other for a long time period. To do this, the researchers brought together mice from a German population and mice from a French population. Although to begin with all the mice mated with one another randomly, the hybrid offspring of French and German parents were distinctly more choosy: they showed a definite preference for mating with individuals from their father's original population. According to the researchers, this paternal imprinting accelerates the divergence of two house mouse populations and thus promotes speciation.In allopatric speciation, individuals of a species become geographically isolated from each other by external factors such as mountains or estuaries. Over time, this geographic separation leads to the sub-populations undergoing various mutations, and thus diverging genetically. Animals from the two different sub-populations can no longer successfully reproduce, so two new species evolve.To find out what role partner selection plays in such speciation processes, Diethard Tautz from the Max Planck Institutefor Evolutionary Biology and his colleagues conducted a comprehensive study on house mice -- the classic model organisms of biology. "To investigate whether there are differences in the mating behaviour of the mice in the early stages of speciation, we caught wild house mice in southern France and western Germany. The two populations have been geographically separate for around 3,000 years, which equates to some 18,000 generations," says Diethard Tautz. Due to this geographical separation, the French and German mice were genetically different.The Plön-based researchers created a semi-natural environment for their investigations -- a sort of "Playboy Mansion" for mice. The research enclosure was several square meters in size and was divided up using wooden walls, "nests" made out of plastic cylinders, and plastic tubes. It also featured an escape tube with several entrances, which led into a cage system nearby. "We constructed the enclosure in such a way that all animals had unimpeded access to all areas, but thanks to the structural divisions were also able to create their own territories or retreat into nests," explains Tautz. "The escape tube was a control element. If the mice retreated to it only very seldom -- as was the case in our experiment -- then we could be sure there was no overpopulation in the central enclosure."In this central enclosure, the French and German mice had both time and space to mate with each other and reproduce. "At first, all the mice mated with each other quite randomly. But with the first-generation offspring, a surprising pattern emerged," says Tautz. When the first-generation hybrid offspring of mixed French and German parentage mated, they showed a specific preference for pure-bred mates whose "nationality" was that of their father only. "There must be some kind of paternal influence that prompts the hybrid mice to choose a mate from a specific population, namely that of their father," concludes the biologist, based on the results of his study. "This imprinting must be learned, however, meaning that the animals must grow up in the presence of their fathers. This was not the case for the original mice, which were kept in cages for a time after being caught.""We know that mice use ultrasonic vocalizations to communicate with each other and that particularly in the case of male mice these vocalizations can reveal signals of individuality and kinship. We believe that, like birdsong, the vocalizations of the males have a learned component and a genetic component," says Tautz. Therefore, French and German mice really could "speak" different languages, partly learned from their fathers, partly inherited from them. Individual mice thus have a mating preference for mice that speak the same language as they do.The French and German mouse populations had evidently been geographically separated long enough for preliminary signs of species differentiation to be apparent as regards mating preferences. In addition, another aspect of mating behavior also sped up the speciation process. Although mice have multiple mates, the researchers found evidence of partner fidelity and inbreeding. The tendency to mate with relatives fosters the creation of genetically uniform groups. When both occur together, this accelerates the speciation process.In a next step, Diethard Tautz wants to find out whether the vocalizations of the mice play the decisive role in paternal imprinting, or if scent cues are also involved. Furthermore, the biologist wants to identify the genes that are involved in mate selection. | Genetically Modified | 2,013 |
March 27, 2013 | https://www.sciencedaily.com/releases/2013/03/130327133523.htm | Caffeine-'addicted' bacteria: Finding may lead to new decontamination methods, new medicines | Some people may joke about living on caffeine, but scientists now have genetically engineered | Jeffrey E. Barrick and colleagues note that caffeine and related chemical compounds have become important water pollutants due to widespread use in coffee, soda pop, tea, energy drinks, chocolate and certain medications. These include prescription drugs for asthma and other lung diseases. The scientists knew that a natural soil bacterium, The study reports their success in doing so, as well as use of the The author and co-authors acknowledge financial support from the University of Texas at Austin and the University of Iowa. | Genetically Modified | 2,013 |
March 21, 2013 | https://www.sciencedaily.com/releases/2013/03/130321204809.htm | Researchers alter mosquito genome with goal of controlling disease | Virginia Tech researchers successfully used a gene disruption technique to change the eye color of a mosquito -- a critical step toward new genetic strategies aimed at disrupting the transmission of diseases such as dengue fever. | Zach Adelman and Kevin Myles, both associate professors of entomology in the College of Agriculture and Life Sciences and affiliated researchers with the Fralin Life Science Institute, study the transmission of vector-borne diseases and develop novel methods of control, based on genetics.In a groundbreaking study published this week in the journal While TALENS have been previously used to edit the genomes of animal and human cell cultures, applying them to the mosquito genome is a new approach, according to Adelman."Unlike model organisms with large collections of mutant strains to draw upon, the lack of reverse genetic tools in the mosquito has made it is very difficult to assign functions to genes in a definitive manner," Adelman said. "With the development of this technology, our understanding of the genetic basis of many critical behaviors such as blood-feeding, host-seeking and pathogen transmission should be greatly accelerated."To test the capability of TALENs to specifically edit the mosquito genome, the scientists designed a pair of TALENS to target a gene whose protein product is essential to the production of eye pigmentation in Aedes aegypti, a mosquito species known for its transmission of the viruses that cause dengue fever.Using the TALEN pair to edit the gene in the mosquito's germ cells early in development, they were able to change the eye color of a large percentage of the mosquitoes arising in the next generation from black to white."To date, efforts to control dengue transmission through genetics have focused entirely on adding material to the mosquito genome. Ensuring that this added material is expressed properly and consistently has been a challenge," Adelman said. "This technology allows us to pursue the same goals, namely, the generation of pathogen-resistant mosquitoes, through subtraction. For example, removing or altering a gene that is critical for pathogen replication.""Aedes mosquitoes have become increasingly important as vectors of disease from a public health perspective," said George Dimopoulos, a professor of molecular microbiology and immunology at John Hopkins University who was not involved in the study. "The lack of vaccines and drugs for dengue has left the mosquitoes that carry the virus as one of the most promising targets for controlling the disease. A better understanding of how the virus infects the mosquito and other biological properties of the insect will be required to develop intervention strategies that can block virus transmission by the mosquito. The ability to genetically engineer mosquitoes is essential for the study of such biological functions. The TALEN-based system in mosquitoes that that was developed by Dr. Adelman provides this important capacity."Co-authors of the study include Azadeh Aryan, a Ph.D. student in the department of entomology in the College of Agriculture and Life Sciences, and Michelle A.E. Anderson, a research technician in the department of entomology in the College of Agriculture and Life Sciences. | Genetically Modified | 2,013 |
March 19, 2013 | https://www.sciencedaily.com/releases/2013/03/130319144154.htm | Tomatoes that mimic actions of good cholesterol created | UCLA researchers have genetically engineered tomatoes to produce a peptide that mimics the actions of good cholesterol when consumed. | Published in the April issue of the "This is one of the first examples of a peptide that acts like the main protein in good cholesterol and can be delivered by simply eating the plant," said senior author Dr. Alan M. Fogelman, executive chair of the department of medicine and director of the atherosclerosis research unit at the David Geffen School of Medicine at UCLA. "There was no need to isolate or purify the peptide -- it was fully active after the plant was eaten."After the tomatoes were eaten, the peptide surprisingly was found to be active in the small intestine but not in the blood, suggesting that targeting the small intestine may be a new strategy to prevent diet-induced atherosclerosis, the plaque-based disease of the arteries that can lead to heart attacks and strokes.Specifically for the study, the team genetically engineered tomatoes to produce 6F, a small peptide that mimics the action of apoA-1, the chief protein in high-density lipoprotein (HDL or "good" cholesterol). Scientists fed the tomatoes to mice that lacked the ability to remove low-density lipoprotein (LDL or "bad" cholesterol) from their blood and readily developed inflammation and atherosclerosis when consuming a high-fat diet.The researchers found that mice that ate the peptide-enhanced tomatoes, which accounted for 2.2 percent of their Western-style, high-fat diet, had significantly lower levels of inflammation; higher paraoxonase activity, an antioxidant enzyme associated with good cholesterol; higher levels of good cholesterol; decreased lysophosphatidic acid, a tumor-promoter that accelerates plaque build-up in the arteries in animal models; and less atherosclerotic plaque.Several hours after the mice finished eating, the intact peptide was found in the small intestine, but no intact peptide was found in the blood. According to researchers, this strongly suggests that the peptide acted in the small intestine and was then degraded to natural amino acids before being absorbed into the blood, as is the case with the other peptides and proteins in the tomato."It seems likely that the mechanism of action of the peptide-enhanced tomatoes involves altering lipid metabolism in the intestine, which positively impacts cholesterol," said the study's corresponding author, Srinavasa T. Reddy, a UCLA professor of medicine and of molecular and medical pharmacology.Previous studies performed by Fogelman's lab and other researchers around the world in animal models of disease have suggested that a large number of conditions with an inflammatory component -- not just atherosclerosis -- might benefit from treatment with an apoA-1 mimetic peptide, including Alzheimer's disease, ovarian and colon cancer, diabetes, asthma, and other disorders.The immune system normally triggers an inflammatory response to an acute event such as injury or infection, which is part of the natural course of healing. But with many chronic diseases, inflammation becomes an abnormal, ongoing process with long-lasting deleterious effects in the body.If the work in animal models applies to humans, said Fogelman, who is also the Castera Professor of Medicine at UCLA, consuming forms of genetically modified foods that contain apoA-1-related peptides could potentially help improve these conditions.The peptide would be considered a drug if given by injection or in a purified pill form, but when it is a part of the fruit of a plant, it may be no different from a safety standpoint than the food in which it is contained -- and it may be better tolerated than a drug, Fogelman said. He noted that one possibility could be the development of the peptide into a nutritional supplement.The current study and findings resulted from years of detective work in searching for an apoA-1 peptide that could be practically produced. Peptides prior to the current 6F version have required additions that can only be made by chemical synthesis. The 6F peptide does not require these additions and can therefore be produced by genetically engineering plants.The team chose a fruit -- the tomato -- that could be eaten without requiring cooking that might break down the peptide. The researchers were able to successfully genetically express the peptide in tomato plants, and the ripened fruit was then freeze-dried and ground into powder for use in the study."This is one of the first examples in translational research using an edible plant as a delivery vehicle for a new approach to cholesterol," said Judith Gasson, a professor of medicine and biological chemistry, director of UCLA's Jonsson Comprehensive Cancer Center and senior associate dean for research at the Geffen School of Medicine. "We will be closely watching this novel research to see if these early studies lead to human trials."In addition, Gasson noted that this early finding and future studies may yield important and fundamental knowledge about the role of the intestine in diet-induced inflammation and atherosclerosis.The study was supported in part by U.S. Public Health Service Research Grants HL-30568 and HL-34343 and by the Laubisch, Castera and M.K. Grey funds at UCLA. Studies on the determination of 6F in intestinal contents and plasma were partially funded by a Network Grant from the Leducq Foundation. | Genetically Modified | 2,013 |
March 13, 2013 | https://www.sciencedaily.com/releases/2013/03/130313112211.htm | Making fuel from bacteria | In the search for the fuels of tomorrow, Swedish researchers are finding inspiration in the sea. Not in offshore oil wells, but in the water where blue-green algae thrive. | The building blocks of blue-green algae – sunlight, carbon dioxide and bacteria – are being used by researchers at KTH Royal Institute of Technology in Stockholm to produce butanol, a hydrocarbon-like fuel for motor vehicles.The advantage of butanol is that the raw materials are abundant and renewable, and production has the potential to be 20 times more efficient than making ethanol from corn and sugar cane.Using genetically-modified cyanobacteria, the team linked butanol production to the algae’s natural metabolism, says Paul Hudson, a researcher at the School of Biotechnology at KTH who leads the research. “With relevant genes integrated in the right place in cyanobacteria’s genome, we have tricked the cells to produce butanol instead of fulfilling their normal function,” he says.The team demonstrated that it can control butanol production by changing the conditions in the surrounding environment. This opens up other opportunities for control, such as producing butanol during specific times of day, Hudson says.Hudson says that it could be a decade before production of biofuel from cyanobacteria is a commercial reality. “We are very excited that we are now able to produce biofuel from cyanobacteria. At the same time we must remember that the manufacturing process is very different from today's biofuels,” he says. “We need to improve the production hundredfold before it becomes commercially viable.Already, there is a demonstrator facility in New Mexico, U.S. for producing biodiesel from algae, which is a more advanced process, Hudson says.One of Sweden's leading biotechnology researchers, Professor Mathias Uhlén at KTH, has overall responsibility for the project. He says that the use of engineering methods to build genomes of microorganisms is a relatively new area. A bacterium that produces cheap fuel by sunlight and carbon dioxide could change the world.Hudson agrees. “One of the problems with biofuels we have today, that is, corn ethanol, is that the price of corn rises slowly while jumping up and down all the time and it is quite unpredictable,” he says. “In addition, there is limited arable land and corn ethanol production is also influenced by the price of oil, since corn requires transport. “Fuel based on cyanobacteria requires very little ground space to be prepared. And the availability of raw materials - sunlight, carbon dioxide and seawater - is in principle infinite,” Hudson says.He adds that some cyanobacteria also able to extract nitrogen from the air and thus do not need any fertilizer.The next step in the research is to ensure that cyanobacteria produce butanol in larger quantities without it dying of exhaustion or butanol, which they cannot withstand particularly well. After that, more genes will have to be modified so that the end product becomes longer hydrocarbons that can fully function as a substitute for gasoline. And finally, the process must be executed outside of the lab and scaled up to work in industry.There are also plans to develop fuel from cyanobacteria that are more energetic and therefore particularly suitable for aircraft engines.The project is formally called Forma Center for Metabolic Engineering, and it involves researchers Chalmers University in Sweden. It has received about EUR 3 million from the nonprofit Council Formas. | Genetically Modified | 2,013 |
March 13, 2013 | https://www.sciencedaily.com/releases/2013/03/130313095427.htm | Indirect side-effects of the cultivation of genetically modified plants | Genetically modified Bt cotton plants contain a poison that protects them from their most significant enemies. As a result, these plants rely less on their own defence system. This benefits other pests, such as aphids. These insights stem from a study supported by the Swiss National Science Foundation (SNSF). | Just ten years ago, genetically modified cotton grew on 12% of all fields -- today it is cultivated on over 80% of all cotton fields around the world. Bt cotton contains a gene of Bacillus thuringiensis, a species of soil bacteria. The plant uses it to produce a poison whose effects are fatal to the principal cotton pests -- voracious caterpillars. However, certain types of bugs and other pests begin to spread across cotton fields instead, as is the case in China. The decline in the use of chemical pesticides may be partly responsible for this development, but it is probably not the only factor.A team of researchers led by Jörg Romeis from the Agroscope Reckenholz-Tänikon Research Station has now identified a biological mechanism that offers an additional explanation for the increase in new pests in Bt cotton fields. Cotton plants have a sophisticated defence system. When caterpillars begin to nibble on them, they form defensive substances, so-called terpenoids. This spoils the appetite of not only the caterpillars, but of many other nibblers as well.Cotton aphids generally do not cause severe agricultural damage because they succumb to their natural enemies out in the open. His results are therefore not relevant to farming, says Romeis. However, he has for the first time revealed an indirect effect of Bt cotton: the killing of the caterpillars also affects other plant-eating insects because the plants' defence system remains inactive. Romeis now wants to investigate whether this effect is relevant to aphids only or also to the bugs that are creating problems for cotton farmers in China and in other cotton-growing regions of the world. | Genetically Modified | 2,013 |
March 12, 2013 | https://www.sciencedaily.com/releases/2013/03/130312134733.htm | Some bacteria may protect against disease caused by stomach infection | Half of the world's human population is infected with the stomach bacteria called | "People tend to think of the stomach as a relatively sterile environment, but it's actually populated with microbes," said Karen Ottemann, professor and chair of microbiology and environmental toxicology at UC Santa Cruz.Researchers in Ottemann's lab were studying "We found that something about the preexisting microflora, before The findings, published in the journal "It would be nice if we could predict who would get disease," Ottemann said. "The other possibility is that we might be able to identify some bacteria that could be used as a probiotic to dampen At this point, it is not clear which bacteria are responsible for changing the response to The researchers treated some of the mice with antibiotics, which did not eliminate stomach bacteria but substantially changed the composition of the gut microflora. The altered microflora dampened the inflammatory response to More work is needed to identify which differences in bacterial composition are responsible for the differences in response to In addition to Ottemann, the coauthors of the paper include first author Annah Rolig, a graduate student in Ottemann's lab; undergraduates Cynthia Cech and Ethan Ahler; and J. Elliott Carter, a pathologist at the University of South Alabama College of Medicine. This research was funded by the National Institute of Allergy and Infectious Disease (NIAID) at the National Institutes of Health (grant #AI050000) and the UC Cancer Research Coordinating Committee. | Genetically Modified | 2,013 |
March 7, 2013 | https://www.sciencedaily.com/releases/2013/03/130307145109.htm | Biologists produce rainbow-colored algae | What can green algae do for science if they weren't, well, green? | That's the question biologists at UC San Diego sought to answer when they engineered a green alga used commonly in laboratories, While fluorescent green, red, blue and yellow may be all the rage this year for running shoes and other kinds of sporting gear, fluorescent algae hasn't been a style trend yet in scientific laboratories. But in announcing their achievement in the current issue of Although rainbow colored algae are not likely to end up in a store near you any time soon, the scientists say they are powerful tools that will allow biologists working on algae to make biotechnology developments more rapidly, ultimately leading to the production of lower-cost biofuels and cheaper human and animal therapeutics. Several months ago, biologists in the same UC San Diego laboratory reported genetically engineering The rainbow-colored algae were developed by a collaboration that included scientists from the University of Nebraska, Lincoln. Beth Rasala, a postdoctoral fellow in Mayfield's laboratory, is the lead author of | Genetically Modified | 2,013 |
March 7, 2013 | https://www.sciencedaily.com/releases/2013/03/130307124808.htm | Protein lost in tumors blocks normal cells from being reprogrammed into stem cells | Researchers from the Icahn School of Medicine at Mount Sinai have discovered that a particular protein prevents normal cells from being reprogrammed into cells that resemble stem cells, providing new insight into how they may lose their plasticity during normal development. This finding has broad-reaching implications for how cells change during both normal and disease development. | The data are published this week in In a previous study, Emily Bernstein, PhD, and her team at Mount Sinai studied the natural progression of melanoma using mouse and human cells, as well as patient samples, and found that the loss of a specific histone variant called macroH2A, which is a protein that helps package DNA, was directly related to the growth and metastasis of melanoma. In the current study, her team wanted to find out how this molecule might act as a barrier to cellular reprogramming. The importance of cellular reprogramming has been recently highlighted by the winners of the Nobel Prize of Medicine (2012), and explores the capacity of reversing adult cells to an early stage of development, the so called embryonic stem cell.Working with researchers at the University of Pennsylvania, Dr. Bernstein evaluated mice that were genetically engineered to lack macroH2A in comparison to control or "wild-type" mice. They used skin cells from these mice and attempted to reprogram the cells in petri dishes into pluripotent cells. They found that the cells derived from mice without macroH2A were much more plastic, meaning they were more easily reprogrammed into stem-like cells, compared to the wild-type mice. This indicates that macroH2A may block cellular reprogramming by silencing genes required for plasticity."This is the first evidence of the involvement of a histone variant protein as an epigenetic barrier to induced pluripotency (iPS) reprogramming," said Dr. Bernstein, who is an Assistant Professor of Oncological Sciences and Dermatology at the Graduate School of Biomedical Sciences at Mount Sinai, and corresponding author of the study. "These findings help us to understand the progression of different cancers and how macroH2A might be acting as a barrier to tumor development."Next, Dr. Bernstein and her team plan to create cancer cells in a petri dish by manipulating healthy cells with genetic mutations often associated with cancer, coupled to removal of macroH2A to examine whether the cells are capable of forming tumors.This study was supported by funding from a New York State Stem Cell Science Award (C024285) and a National Institutes of Health Grant (R01CA154683). | Genetically Modified | 2,013 |
March 7, 2013 | https://www.sciencedaily.com/releases/2013/03/130307124802.htm | Scientists improve transgenic 'Enviropigs' | A research team at the University of Guelph has developed a new line of transgenic "Enviropigs." The new line of pigs is called the Cassie line, and it is known for passing genes on more reliably. The results of this project were published ahead of print in the | Enviropigs have genetically modified salivary glands, which help them digest phosphorus in feedstuffs and reduce phosphorus pollution in the environment. After developing the initial line of Enviropigs, researchers found that the line had certain genes that could be unstable during reproduction or impractical in commercial use.Scientists at the University of Guelph created the Cassie line to address these problems. In their paper for the Phosphorus is crucial for healthy growth in pigs. Unfortunately, 50 to 70 percent of the phosphorus in grain is in the form of phytic acid, a compound indigestible by pigs. Because of this, many farmers have to supplement pig diets with an enzyme called phytase. Phytase breaks down phytic acid and helps pigs digest more of the nutrient. The phytase enzyme has a hefty price tag for farmers, and the enzyme can be accidentally damaged or destroyed when farmers mix feed.The Enviropig was created to solve this problem. The transgenic pig synthesizes phytase in its salivary glands, eliminating the need for additional supplements or enzymes in the feed. By digesting more phosphorus, the Enviropig also produces less phosphorus in its waste."The enzyme is secreted in the saliva and functions in a similar fashion to that of phytase included in the diet," said Dr. Cecil Forsberg, Professor Emeritus, Department of Molecular and Cell Biology at the University of Guelph and co-author of the study.Though no studies indicate a food safety risk from genetically modified Enviropig pork, meat from the Enviropig is not yet available for human consumption. Forsberg said using Enviropigs could improve food production and the environment."When transgenic food animals are accepted by consumers, the Enviropig perhaps would be one of the first innovations to be introduced into swine production," said Forsberg. "We have demonstrated that the gene can be transferred by breeding through many generations in a stable fashion. Furthermore, the pigs are healthy."Research on the Cassie line stopped in June 2012, but researchers collected semen from the pigs, and they have the option to breed new Enviropigs. | Genetically Modified | 2,013 |
March 5, 2013 | https://www.sciencedaily.com/releases/2013/03/130305174653.htm | Spinal tap -- using cactus spines to isolate DNA | Isolation of DNA from some organisms is a routine procedure. For example, you can buy a kit at your local pharmacy or grocery store that allows you to swab the inside of your cheek and send the sample for DNA sequencing. However, for other organisms, DNA extraction is much more problematic. Researchers at Desert Botanical Garden in Phoenix, Arizona, have developed a novel procedure that greatly simplifies genomic DNA isolation from cactus tissue. | For members of the family Cactaceae, isolation of genetic material can be difficult due to the presence of polysaccharide-based mucilage content and other secondary compounds. Although important for water storage, these compounds necessitate the use of toxic chemicals and numerous modifications to protocols for DNA extraction. Lead author Shannon D. Fehlberg and colleagues describe a novel method for isolation of DNA using cactus spines in the March issue of "I had worked with getting DNA out of cactus in the past where you use pieces of the epidermis, but it was messy and difficult to sample. It was also difficult to deal with in the lab because of the mucilage," says Fehlberg. "Now you can snip a spine and, while you have to grind the spine up, it is easy to collect and easy to store and you can follow the manufacturer's protocols for extraction -- simplifying both the field and genetic work."Considered to be modified leaves, spines contain significantly less mucilage content compared to other tissues commonly used for sampling in Cactaceae. Additionally, removal of cactus spines is less invasive than sampling epidermal tissue, which can damage plants and expose the underlying soft tissue to pathogens."Although you can cut a fairly small sample of epidermal tissue, this can be problematic if you are working with living collections or endangered species. Not only is it much easier to clip a spine, it is also more aesthetic and less harmful," comments Fehlberg.As the cost of DNA sequencing has dramatically decreased, its use has grown exponentially. Because it allows the comparison of individuals within and between populations, DNA sequencing has played an important role in understanding genetic diversity. "For example, in the plant species I'm studying, the species boundaries are not clear," says Fehlberg. "Genetics is important for determining what can be considered a cohesive group. "Knowledge of genetic variation among populations will provide insight to the persistence of a species and inform conservation efforts. Fehlberg notes, "Genetics is helpful in determining how similar populations are to one another and how connected they are. We're able to use both genetics and biological information to determine which populations are most unique and which are most threatened." | Genetically Modified | 2,013 |
March 5, 2013 | https://www.sciencedaily.com/releases/2013/03/130305154531.htm | Why fish is better than supplements: Omega-3s from fish vs. fish oil pills better at maintaining blood pressure in mouse model | Omega-3 fatty acids found in oily fish may have diverse health-promoting effects, potentially protecting the immune, nervous, and cardiovascular systems. | But how the health effects of one such fatty acid -- docosahexaenoic acid (DHA) -- works remains unclear, in part because its molecular signaling pathways are only now being understood.Toshinori Hoshi, PhD, professor of Physiology, at the Perelman School of Medicine, University of Pennsylvania, and colleagues showed, in two papers out this week in the The researchers found that DHA rapidly and reversibly activates these channels by increasing currents by up to 20 fold. DHA lowers blood pressure in anesthetized wild type mice but not in mice genetically engineered without a specific ion channel subunit.In comparison, the team found that a dietary supplement, DHA ethyl ester, found in most fish oil pills fails to activate the same channels, and even antagonizes the positive effect of DHA from natural sources, on the cells. The DHA ethyl ester seems to compete with the natural form of DHA for binding sites on the ion channel.The team concluded that these channels have receptors for long-chain omega-3 fatty acids, and that DHA -- unlike its ethyl ester cousin -- activate the channels and lower blood pressure.The findings have practical implications for the use of omega-3 fatty acids as nutraceuticals for the general public and also for critically ill patients who may receive omega-3-enriched formulas as part of their nutrition.Coauthor Michael Bauer from Jena University Hospital in Germany, who studies sepsis in a clinical setting, says the findings may encourage physicians to have a closer look at the specific formulations given to sepsis patients as they may contain either the free omega-3 acid or the ester.The findings also underscore the importance of obtaining omega-3 fatty acids from natural food sources such as oily fish.The study was supported, in part, by the National Institutes of Health (R01GM057654), the German Research Foundation, and Natural Science Foundation of China. | Genetically Modified | 2,013 |
March 5, 2013 | https://www.sciencedaily.com/releases/2013/03/130305080747.htm | Viruses: More survival tricks than previously thought | For what may be the first time, researchers have discovered a virus inside a host with a non-standard nuclear genetic code -- one that differs from the standard genetic code that almost all living things use to produce proteins. | "The finding is significant because it shows that these viruses can overcome what appears to be an insurmountable change in the host genome," said researcher Derek J. Taylor, professor of biological sciences at the University at Buffalo. "So the fact that we haven't previously seen any viruses in these species with a modified genetic code may not be because the viruses can't adapt to that shift. It may be that we haven't looked hard enough."Taylor's co-authors on the study are UB PhD candidate Matthew Ballinger, former UB postdoctoral researcher Shaun M. Bowman, and UB Professor Jeremy Bruenn, all in UB's Department of Biological Sciences.The team of scientists discovered the highly adapted virus -- a totivirus -- in the yeast species In most living things, the genetic code comprises 64 elements called codons, most of which instruct the body to produce a certain amino acid, the basic building block of a protein. In It had been thought that such a radical change in the genome may help host species evade viruses, which rely on hosts' genetic machinery to create new viral proteins and replicate.However, the presence of the totivirus in While viruses have previously been shown to infect organelles known as mitochondria with a different genetic code, this appears to be the first time a virus has been found to use the modified nuclear code of a complex, cellular host, Taylor said. Whereas the origins of the mitochondrial viruses remain mysterious, the current study was able to reconstruct the origins of the novel yeast virus.The research team found a variety of odd and interesting evidence pointing to a history of co-evolution between totiviruses and yeasts with the modified code. For instance, the modified yeasts appeared to have incorporated genetic material from totiviruses into their genomes on at least four occasions. In total, evidence was found of past, or present, viral infection in five lineages of yeasts with a modified genetic code.In the yeast "It's a non-retroviral RNA virus gene being kidnapped and expressed as a protein by a cellular host in the absence of a current viral infection" Taylor said. The function of this protein is unknown, but the result is further evidence of the unexpected co-evolution between viruses and hosts with modified nuclear code. | Genetically Modified | 2,013 |
February 28, 2013 | https://www.sciencedaily.com/releases/2013/02/130228124134.htm | Fighting GM crop vandalism with a government-protected research site | Genetically modified (GM) crops have been a source of great controversy -- particularly in Europe -- but acts of vandalism and associated security costs have made scientific evidence about the health and ecological impacts of those crops hard to come by. A Swiss government-protected field site dedicated for use in GM crop studies could serve as an example to other European countries interested in pursuing crop biotechnology, according to an article published Feb. 28 in | The protected field site will now enable research groups to conduct experiments without having to install and pay for security measures. The research station is expected to operate with an annual budget of €600,000."This could be a model for other European countries that wish to evaluate the advantages and disadvantages of GM crops in an objective and scientific manner with less risk of vandalism," said Jörg Romeis of Zurich's Agroscope Reckenholz-Tänikon Research Station.As of 2010, opponents of genetic modification had destroyed more than 100 field trials in Europe. At the Reckenholz site, a group of more than 30 masked activists threatened researchers and destroyed about 30 percent of the experimental plants in a 2008 field trial.The new protected field site will provide GM crop researchers with all the technical security measures needed to guard against such attacks, including perimeter fencing, round-the-clock guarding and surveillance of the experimental field, and an alarm system.Romeis and his colleagues say that vandalism and its associated costs appear to be a major factor in the steady decline of European GM research, a situation that they call unacceptable.In many parts of the world, GM crops are gaining popularity. In 2011, as much as 10 percent of the world's arable crop area was planted with GM crops. However, the adoption of GM plants has been very low in Europe, with only two GM crops approved for cultivation: Bt maize and a starch-modified potato. No GM crop is approved for commercial release in Switzerland, where there is a voter-approved moratorium in place through 2017. However, scientific research, including field experiments with GM plants, is permitted.Romeis says that the establishment of such protected sites could eventually reverse the decline in GM field trials and strengthen plant biotechnology research in Europe. | Genetically Modified | 2,013 |
February 26, 2013 | https://www.sciencedaily.com/releases/2013/02/130226092126.htm | 'Fat worms' inch scientists toward better biofuel production | Fat worms confirm that researchers from Michigan State University have successfully engineered a plant with oily leaves - a feat that could enhance biofuel production as well as lead to improved animal feeds. | The results, published in the current issue of Traditional biofuel research has focused on improving the oil content of seeds. One reason for this focus is because oil production in seeds occurs naturally. Little research, however, has been done to examine the oil production of leaves and stems, as plants don't typically store lipids in these tissues.Christoph Benning, MSU professor of biochemistry and molecular biology, led a collaborative effort with colleagues from the Great Lakes Bioenergy Research Center. The team's efforts resulted in a significant early step toward producing better plants for biofuels."Many researchers are trying to enhance plants' energy density, and this is another way of approaching it," Benning said. "It's a proof-of-concept that could be used to boost plants' oil production for biofuel use as well as improve the nutrition levels of animal feed."Benning and his colleagues began by identifying five genes from one-celled green algae. From the five, they identified one that, when inserted into Arabidopsis thaliana, successfully boosted oil levels in the plant's leaf tissue.To confirm that the improved plants were more nutritious and contained more energy, the research team fed them to caterpillar larvae. The larvae that were fed oily leaves from the enhanced plants gained more weight than worms that ate regular leaves.For the next phase of the research, Benning and his colleagues will work to enhance oil production in grasses and algae that have economic value. The benefits of this research are worth pursuing, Benning said."If oil can be extracted from leaves, stems and seeds, the potential energy capacity of plants may double," he said. "Further, if algae can be engineered to continuously produce high levels of oil, rather than only when they are under stress, they can become a viable alternative to traditional agricultural crops."Moreover, algae can be grown on poor agricultural land -- a big plus in the food vs. fuel debate, he added."These basic research findings are significant in advancing the engineering of oil-producing plants," said Kenneth Keegstra, GLBRC scientific director and MSU University Distinguished Professor of biochemistry and molecular biology. "They will help write a new chapter on the development of production schemes that will enhance the quantity, quality and profitability of both traditional and nontraditional crops."Additional MSU researchers and GLBRC members contributing to the study include Gregg Howe, biochemistry and molecular biology professor; John Olhrogge, University Distinguished Professor of plant biology; and Gavin Reid, biochemistry and molecular biology associate professor. | Genetically Modified | 2,013 |
February 21, 2013 | https://www.sciencedaily.com/releases/2013/02/130221104353.htm | Omega-3s inhibit breast cancer tumor growth, study finds | A lifelong diet rich in omega-3 fatty acids can inhibit growth of breast cancer tumours by 30 per cent, according to new research from the University of Guelph. | The study, published recently in the "It's a significant finding," said David Ma, a professor in Guelph's Department of Human Health and Nutritional Sciences, and one of the study's authors."We show that lifelong exposure to omega-3s has a beneficial role in disease prevention -- in this case, breast cancer prevention. What's important is that we have proven that omega-3s are the driving force and not something else."Breast cancer remains the most common form of cancer in women worldwide and is the second leading cause of female cancer deaths.Advocates have long believed diet may significantly help in preventing cancer. But epidemiological and experimental studies to back up such claims have been lacking, and human studies have been inconsistent, Ma said."There are inherent challenges in conducting and measuring diet in such studies, and it has hindered our ability to firmly establish linkages between dietary nutrients and cancer risk," he said."So we've used modern genetic tools to address a classic nutritional question."For their study, the researchers created a novel transgenic mouse that both produces omega-3 fatty acids and develops aggressive mammary tumours. The team compared those animals to mice genetically engineered only to develop the same tumours."This model provides a purely genetic approach to investigate the effects of lifelong omega-3s exposure on breast cancer development," Ma said."To our knowledge, no such approach has been used previously to investigate the role of omega-3s and breast cancer."Mice producing omega-3s developed only two-thirds as many tumours -- and tumours were also 30-per-cent smaller -- as compared to the control mice."The difference can be solely attributed to the presence of omega-3s in the transgenic mice -- that's significant," Ma said."The fact that a food nutrient can have a significant effect on tumour development and growth is remarkable and has considerable implications in breast cancer prevention."Known as an expert in how fats influence health and disease, Ma hopes the study leads to more research on using diet to reduce cancer risk and on the benefits of healthy living."Prevention is an area of growing importance. We are working to build a better planet, and that includes better lifestyle and diet," he said."The long-term consequences of reducing disease incidence can have a tremendous effect on the health-care system."The study also involved lead author Mira MacLennan, a former U of G graduate student who is now studying medicine at Dalhousie University; U of G pathobiology professor Geoffrey Wood; former Guelph graduate students Shannon Clarke and Kate Perez; William Muller from McGill University; and Jing Kang from Harvard Medical School.Funding for this research came from the Canadian Breast Cancer Research Alliance/Canadian Institutes of Health Research, the Canada Foundation for Innovation and the Ontario Research Fund. | Genetically Modified | 2,013 |
February 17, 2013 | https://www.sciencedaily.com/releases/2013/02/130217134218.htm | Genetically modified crops are overregulated, food science expert says | It has been almost 20 years since the first genetically modified foods showed up in produce aisles throughout the United States and the rest of the world, but controversy continues to surround the products and their regulation. | Bruce Chassy, a professor emeritus of food science and human nutrition at the University of Illinois at Urbana-Champaign, believes that after thousands of research studies and worldwide planting, "genetically modified foods pose no special risks to consumers or the environment" and are overregulated.Chassy elaborated on this conclusion at the 2013 meeting of the American Association for the Advancement of Science in Boston on Feb. 17. During his talk, "Regulating the Safety of Foods and Feeds Derived From Genetically Modified Crops," Chassy shared his view that the overregulation of GM crops actually hurts the environment, reduces global health and burdens the consumer.Farmers have witnessed the advantages of GM crops firsthand through increases in their yields and profit, and decreases in their labor, energy consumption, pesticide use and greenhouse gas emissions, Chassy said.Despite these benefits, various regulatory agencies require newly developed GM crops to be put to the test with rigorous safety evaluations that include molecular characterization, toxicological evaluation, allergenicity assessments, compositional analysis and feeding studies. This extensive testing takes five to 10 years and costs tens of millions of dollars, and Chassy argues that this process "wastes resources and diverts attention from real food safety issues.""With more than half of the world's population now living in countries that have adopted GM crops, it might be appropriate to reduce the regulatory scrutiny of GM crops to a level that is commensurate with science-based risk assessment," Chassy said.During his talk, Chassy chronicled the scientific tests used in pre-market safety assessments of GM foods and elaborate on the evidence from thousands of research studies and expansive GM plantings that he says show these crops do not present risks to consumers or the environment. The overregulation of GM foods is a response not to scientific evidence, Chassy said, but to a global campaign that disseminates misinformation and fear about these food sources. | Genetically Modified | 2,013 |
February 17, 2013 | https://www.sciencedaily.com/releases/2013/02/130217085025.htm | Avoiding virus dangers in 'domesticating' wild plants for biofuel use | In our ongoing quest for alternative energy sources, researchers are looking more to plants that grow in the wild for use in biofuels, plants such as switchgrass. | However, attempts to "domesticate" wild-growing plants have a downside, as it could make the plants more susceptible to any number of plant viruses.In a presentation at this year's meeting of the American Association for the Advancement of Science, Michigan State University plant biologist Carolyn Malmstrom said that when we start combining the qualities of different types of plants into one, there can be unanticipated results."Most wild plants are perennials, while most of our agriculture crops are annuals," Malmstrom said. "Sometimes when you mix the properties of the two, unexpected things can happen."For example, annual domestic plants are made to grow quickly. "In agriculture we select more for growth," she said. "There is a reduced need for the plants to defend themselves because we have taken care of that."If pest control measures aren't taken, these annual plants can serve as "amplifiers," producing lots of viruses and insects to move the viruses around.In contrast, perennial plants in nature grow slower, but are usually better equipped to fight off invading viruses. When wild-growing perennials do get infected they can serve as reservoirs for viruses, Malmstrom said, "a place where viruses can hang out a long time."In the domestication of wild plants for bioenergy, long-lived plants are being selected for fast growth like annuals. "Now you have a plant that could be a long-term reservoir, but it also happens to be faster growing and can serve as an amplifier for viruses. This all-in-one combination could increase virus pressure in crop areas unless mitigated."Malmstrom said that plant virus ecology and the study of viral interactions between wild-growing plants and agricultural crops is an expanding field. In the last 15 years, disease ecology has really come to the fore as a basic science.Most of what is known about plant viruses comes from studies of crops. To understand the complete ecology of viruses, researchers are now studying these tiny organisms in nature, too. "The mysteries of how plant viruses can play a role in ecosystem properties and processes in natural ecosystems are emerging more slowly," Malmstrom said.Malmstrom said it's important to catch-up in our understanding of viral ecology, as there are any number of societal issues that need to be addressed in this area."Society wants us to be able to answer questions such as whether viruses can be used in agricultural terrorism, how to recognize a novel virus, and what happens if a virus is genetically modified and then let loose?" | Genetically Modified | 2,013 |
February 14, 2013 | https://www.sciencedaily.com/releases/2013/02/130214194101.htm | The human pathogen Streptococcus pneumonia shields foreign DNA derived from other bacteria to promote genetic diversity and vaccine evasion | A new report demonstrates that the human pathogen | This study, published February 14 in the Open Access journal Exchange of pathogenicity islands is crucial for pneumococcal virulence, as illustrated by the impressive variability in the polysaccharide capsule, which is usually targeted by current vaccines. Acquisition of different capsule loci, by relying on this genetic transformation, thus allows for vaccine evasion. Natural genetic transformation is thought of as the bacterial equivalent of sexual reproduction, allowing intra- and inter-species genetic exchange. This process, involving uptake of foreign DNA as single-strands (ss) that leads to chromosomal integration, is transient in Restriction-modification (R-M) systems classically include a restrictase, which protects the host bacteria from attack by bacteriophage via the degradation of only the foreign double-stranded (ds) DNA, and a dsDNA methylase that methylates the host genome, providing self-immunity against this restrictase. Since they degrade only foreign DNA, R-M systems are proposed to antagonize transformation by DNA from other bacteria. The DpnII R-M system investigated in this study is present in around half of pneumococcal isolates tested and also possesses an unusual methylase of ssDNA, DpnA, which is specifically induced during the brief genetic transformation time window.This study shows that DpnA gene is crucial for the exchange of pathogenicity islands when the foreign DNA is unmethylated (i.e., from a non-DpnII modified DNA donor). By methylating the internalized foreign ssDNA, DpnA protects the chromosome of those transformants that incorporate the foreign pathogenicity islands, such as the capsule locus. In the absence of this unique methylation, the novel transformant chromosomes would be degraded by the DpnII restrictase, thus forbidding the acceptance of the foreign DNA sequences.The researchers found that the role of DpnA is to protect foreign DNA, allowing pathogenicity island exchange between bacteria. Jean-Pierre Claverys, Principal Investigator and senior author of the paper concludes that "this finding is the first evidence for a mechanism that actively promotes genetic diversity of | Genetically Modified | 2,013 |
February 14, 2013 | https://www.sciencedaily.com/releases/2013/02/130214133922.htm | Studies reveal genetic variation driving human evolution | A pair of studies published Feb. 14 by Cell Press in the journal | "There is an archaeological record hidden in our DNA that can help point us to the traits that have been critical in human survival, such as resistance to infectious diseases and new abilities to respond to different environments," says senior study author Pardis Sabeti of Harvard University and the Broad Institute. "The two studies have uncovered two intriguing human adaptive traits and demonstrate the ability to go from an unbiased genome scan to a novel hypothesis of human evolution."Sabeti and her team found that a previously reported variant of the EDAR gene, which arose in central China about 30,000 years ago, increased the number of sweat glands in genetically modified mice and had other effects not previously reported in humans; their discovery demonstrates that animal models can be used to study the biological changes expected to result from human genetic variation. This gene variant was also associated with an increase in the number of sweat glands in a present-day Han Chinese population. By enhancing sweating, this EDAR variant could have helped humans adapt to humid climates that may have existed in China 30,000 years ago.In the accompanying study, the researchers used data from the 1000 Genomes Project to analyze DNA sequence variations across the entire genome. They identified hundreds of gene variants that potentially contributed to human evolutionary adaptation. One of these variants, a mutation in the TLR5 gene, changed the immune responses of cells exposed to bacterial proteins, suggesting that this variant could confer a fitness advantage by protecting against bacterial infections. The comprehensive list of possible adaptive mutations driving recent human evolution provides the groundwork for future studies.Together, the two studies represent a decisive shift for the field of evolutionary genomics, transitioning from hypothesis-driven to hypothesis-generating science. By moving from genome-wide scans to the characterization of adaptive mutations, it is possible to elucidate distinct mechanisms of evolution."These two studies are the product of work done in this area for over a decade but can only now be made possible with the major breakthroughs in genomic technology," Sabeti says. "I am struck by the ability of genomics to uncover the secrets of human history." | Genetically Modified | 2,013 |
February 7, 2013 | https://www.sciencedaily.com/releases/2013/02/130207172100.htm | Colon cancer exhibits a corresponding epigenetic pattern in mice and humans | Tumourigenesis is driven by genetic alterations and by changes in the epigenome, for instance by the addition of methyl groups to cytosine bases in the DNA. A deeper understanding of the interaction between the genetic and epigenetic mechanisms is critical for the selection of tumour biomarkers and for the future development of therapies. Human tumour specimens and cell lines however contain a plethora of genetic and epigenetic changes, which complicate data analysis. In contrast, certain mouse tumour models contain only a single genetic mutation and allow the analysis of nascent tumours. | Scientists of the Max Planck Institute for Molecular Genetics in Berlin have now discovered a recurring pattern of more than 13,000 epigenetic alterations in young tumours of the mouse. This genome-wide pattern was found to be partly conserved in human colon carcinoma, and may therefor facilitate the identification of novel clinical colon cancer biomarkers for early detection.Two kinds of molecular changes are known to trigger tumour development: one is genetic mutations -- i.e. alterations in the alphabetic sequence of the DNA -activating genes that lead to uncontrolled growth of tumours, or inactivating genes that inhibit this growth. The other is epigenetic modifications, for example new distributions of methyl groups in the DNA that contribute to the genetic information in the cancer cells being interpreted differently.Genetic and epigenetic mechanisms work together in cancer development -- but little was known about how these systems mutually influence one another, and which changes first come to light. These questions can only be answered with great difficulty through investigating human tumours: the cancer is usually already several years old when diagnosed. Accordingly, the cancer cells already exhibit thousands of genetic and epigenetic changes at this stage, which complicates the analysis.The matter is different for the corresponding polyps in mice, which the researchers can investigate considerably earlier following their formation. For this reason, scientists of the Max Planck Institute for Molecular Genetics have now pursued the question of which epigenetic changes in intestinal tumours occur first with the help of a mouse model. "With mice, we can investigate the first changes much more easily than with humans," says Markus Morkel, who led the study. The scientists analysed the epigenetic changes in a strain of mice with a defective copy of the APC gene. This gene serves as an intestinal tumour suppressor in mice as well as in humans. Accordingly, it has lost its functionality in a majority of patients with colon cancer.The results displayed a clear picture: The researchers recognised a recurring pattern of more than 13,000 epigenetic changes in all of the mouse tumour samples. By contrast, they did not find this pattern in healthy intestine or in intestinal stem cells, which are the cells of origin of the tumour. Since the mice -and hence the tumours- were less than three months old, the changes must have already spread shortly after the first genetic mutation in the APC gene within the tumour cells. According to the scientists, the first mutation already leads to pathological activation of numerous enzymes controlling the epigenetic mechanisms.Remarkably, the molecular biologists discovered large parts of the tumour-specific epigenetic pattern not only in the mouse, but also in human colon cancer tissue. "These initial epigenetic changes could therefore serve as markers and significantly simplify the early diagnosis of colon tumours in the future," hopes Markus Morkel. Patients would merely have to provide a blood sample for the diagnosis and could forego an enteroscopic procedure. | Genetically Modified | 2,013 |
February 7, 2013 | https://www.sciencedaily.com/releases/2013/02/130207074254.htm | Device made of DNA inserted into bacterial cell works like a diagnostic computer | Scientists hope that one day in the distant future, miniature, medically-savvy computers will roam our bodies, detecting early-stage diseases and treating them on the spot by releasing a suitable drug, without any outside help. To make this vision a reality, computers must be sufficiently small to fit into body cells. Moreover, they must be able to "talk" to various cellular systems. These challenges can be best addressed by creating computers based on biological molecules such as DNA or proteins. The idea is far from outrageous; after all, biological organisms are capable of receiving and processing information, and of responding accordingly, in a way that resembles a computer. | Researchers at the Weizmann Institute of Science have recently made an important step in this direction: They have succeeded in creating a genetic device that operates independently in bacterial cells. The device has been programmed to identify certain parameters and mount an appropriate response.The device searches for transcription factors -- proteins that control the expression of genes in the cell. A malfunction of these molecules can disrupt gene expression. In cancer cells, for example, the transcription factors regulating cell growth and division do not function properly, leading to increased cell division and the formation of a tumor. The device, composed of a DNA sequence inserted into a bacterium, performs a "roll call" of transcription factors. If the results match preprogrammed parameters, it responds by creating a protein that emits a green light -- supplying a visible sign of a "positive" diagnosis. In follow-up research, the scientists -- Prof. Ehud Shapiro and Dr. Tom Ran of the Biological Chemistry and Computer Science and Applied Mathematics Departments -- plan to replace the light-emitting protein with one that will affect the cell's fate, for example, a protein that can cause the cell to commit suicide. In this manner, the device will cause only "positively" diagnosed cells to self-destruct.In the present study, published in Following the success of the study in bacterial cells, the researchers are planning to test ways of recruiting such bacteria as an efficient system to be conveniently inserted into the human body for medical purposes (which shouldn't be a problem; recent research reveals there are already 10 times more bacterial cells in the human body than human cells). Yet another research goal is to operate a similar system inside human cells, which are much more complex than bacteria. | Genetically Modified | 2,013 |
February 4, 2013 | https://www.sciencedaily.com/releases/2013/02/130204153708.htm | Scientists design mouse with more human-like immune response | Medical scientists at USC have bred a first-of-its-kind mouse model that possesses an immune response system more like that of a human's. The discovery makes way for quicker and more cost-effective development of next-generation drugs to treat human diseases, such as cancer, diabetes and tuberculosis. | Medical researchers have long used mice and rats to help formulate new drugs and vaccines, in part because their genetic and biological characteristics closely parallel human physiology. But many experimental drugs that work extraordinarily well in rodents fail miserably when tested in people.One such drug, α-galactosylceramide (α-GalCer), essentially wipes out cancerous tumors in mice by activating the body's immune system; for reasons not entirely clear, the drug does not trigger the same response in people with cancer. Scientists hypothesize that this failure is due to subtle differences between the CD1d molecules in mice and humans and how they respond to tumors and infection. CD1d molecules are found on certain cells that trigger the body's innate immune response.In a study to be published this week by the "It's the best model we have in the field," said Weiming Yuan, assistant professor of molecular microbiology and immunology at the Keck School of Medicine of USC and principal investigator of the study. "We've basically set a platform to fast-track the identification of immunotherapies that can kill cancer and also make vaccines stronger."Once activated, NKT cells react in a matter of hours whereas other T cells may take days. This rapid response makes them difficult to study but also an ideal target for drug-makers. Yuan's humanized mouse allows scientists to more accurately test the viability of those NKT cell-targeting drugs before going to human clinical trials."Before, it would have been a guess as to whether the drug would work in people. Now, the chance of success goes from one out of 100 to one out of five," Yuan said.Yuan and colleagues have yet to demonstrate the effects of inserting a more human-like version of the final component of the CD1d/NKT system, the T cell receptor. More experiments are necessary to determine why α-GalCer is ineffective in treating people with cancer and to develop novel α-GalCer derivatives that work with the human immune system.Co-authors included Xiangshu Wen, Seil Kim and Agnieszka Lawrenczyk of the Keck School; Ping Rao of the UCLA Immunogenetics Center and Department of Pathology; Leandro Carreño and Steven Porcelli of the Albert Einstein College of Medicine at Yeshiva University; and Peter Cresswell of the Yale University School of Medicine.The research was supported by the National Institutes of Health (R01 AI091987, R01 AI059167, R01 AI045889), the Harry Lloyd Charitable Trust, the Margaret Early Medical Research Trust and the Howard Hughes Medical Institute. | Genetically Modified | 2,013 |
February 1, 2013 | https://www.sciencedaily.com/releases/2013/02/130201100244.htm | Genetically modified tobacco plants produce antibodies to treat rabies | Smoking tobacco might be bad for your health, but a genetically altered version of the plant might provide a relatively inexpensive cure for the deadly rabies virus. In a new research report appearing in | "Rabies continues to kill many thousands of people throughout the developing world every year and can also affect international travelers," said Leonard Both, M.Sc., a researcher involved in the work from the Hotung Molecular Immunology Unit at St. George's, University of London, in the United Kingdom. "An untreated rabies infection is nearly 100 percent fatal and is usually seen as a death sentence. Producing an inexpensive antibody in transgenic plants opens the prospect of adequate rabies prevention for low-income families in developing countries."To make this advance, Both and colleagues "humanized" the sequences for the antibody so people could tolerate it. Then, the antibody was produced using transgenic tobacco plants as an inexpensive production platform. The antibody was purified from the plant leaves and characterized with regards to its protein and sugar composition. The antibody was also shown to be active in neutralizing a broad panel of rabies viruses, and the exact antibody docking site on the viral envelope was identified using certain chimeric rabies viruses."Although treatable by antibodies if caught in time, rabies is bad news," said Gerald Weissmann, M.D., Editor-in-Chief of | Genetically Modified | 2,013 |
February 1, 2013 | https://www.sciencedaily.com/releases/2013/02/130201090820.htm | Engineered oncolytic herpes virus inhibits ovarian and breast cancer metastases | A genetically reprogrammed Herpes simplex virus (HSV) can cure metastatic diffusion of human cancer cells in the abdomen of laboratory mice, according to a new study published January 31 in the Open Access journal | Past decades have witnessed significant progress in the ability to treat numerous cancers by means of surgery, chemo- and radio-therapy, or combinations thereof. However, many treatments prolong life for a short time only, or are associated with a poor quality of life.Lead investigator Gabriella Campadelli-Fiume and colleagues re-engineered the entry apparatus of a candidate oncolytic herpesvirus. The reprogrammed virus no longer infects the cells usually targeted by the wild-type virus, nor does it cause herpes-related pathologies. Rather, it acts as a specific weapon against tumor cells that express the HER-2 oncogene."Numerous laboratories worldwide are using viruses as more specific weapons against cancer cells, called oncolytic viruses," says Campadelli-Fiume, Professor of Microbiology and Virology. "Safety concerns prevailed so far, and all oncolytic herpesviruses now in clinical trials are debilitated viruses, effective only against a fraction of tumors. We were the first to obtain a herpes virus reprogrammed to enter HER-2-positive tumor cells, unable to infect any other cell, yet preserves the full-blown killing capacity of the wild-type HSV."Additionally, the laboratory of Pier-Luigi Lollini, Patrizia Nanni and Carla De Giovanni in collaboration with researchers at the Rizzoli Institute, established the new model of human cancer metastases in mice that was used to demonstrate the therapeutic efficacy of the reprogrammed virus.The positive results obtained in the treatment of experimental metastasis hold the promise that the newly retargeted oncolytic HSV described in | Genetically Modified | 2,013 |
January 20, 2013 | https://www.sciencedaily.com/releases/2013/01/130120150035.htm | Developing microbial cell factories by employing synthetic small regulatory RNAs | Biotechnologists have been working hard to address the climate change and limited fossil resource issues through the development of sustainable processes for the production of chemicals, fuels and materials from renewable non-food biomass. One promising sustainable technology is the use of microbial cell factories for the efficient production of desired chemicals and materials. | When microorganisms are isolated from nature, the performance in producing our desired product is rather poor. Metabolic engineering is performed to improve the metabolic and cellular characteristics to achieve enhanced production of desired product at high yield and productivity. Since the performance of microbial cell factory is very important in lowering the overall production cost of the bioprocess, many different strategies and tools have been developed for the metabolic engineering of microorganisms.One of the big challenges in metabolic engineering is to find the best platform organism and to find those genes to be engineered so as to maximize the production efficiency of the desired chemical. Even However, experiment to engineer many genes can be rather difficult due to the time and effort required; for example, gene deletion experiment can take a few weeks depending on the microorganisms. Furthermore, as certain genes are essential or play important roles for the survival of a microorganism, gene knockout experiments cannot be performed. Even worse, there are many different microbial strains one can employ. There are more than 50 different A paper published in Gene expression works like this: the hard-coded blueprint (DNA) is transcribed into messenger RNA (mRNA), and the coding information in mRNA is read to produce protein by ribosomes. Conventional genetic engineering approaches have often targeted modification of the blueprint itself (DNA) to alter organism's physiological characteristics. Again, engineering the blueprint itself takes much time and effort, and in addition, the results obtained cannot be transferred to another organism without repeating the whole set of experiments. This is why Professor Lee and his colleagues aimed at controlling the gene expression level at the translation stage through the use of synthetic small RNA. They created novel RNAs that can regulate the translation of multiple messenger RNAs (mRNA), and consequently varying the expression levels of multiple genes at the same time. Briefly, synthetic regulatory RNAs interrupt gene expression process from DNA to protein by destroying the messenger RNAs to different yet controllable extents. The advantages of taking this strategy of employing synthetic small regulatory RNAs include simple, easy and high-throughput identification of gene knockout or knockdown targets, fine control of gene expression levels, transferability to many different host strains, and possibility of identifying those gene targets that are essential.As proof-of-concept demonstration of the usefulness of this strategy, Professor Lee and his colleagues applied it to develop engineered This new strategy, being simple yet very powerful for systems metabolic engineering, is thus expected to facilitate the efficient development of microbial cell factories capable of producing chemicals, fuels and materials from renewable biomass. | Genetically Modified | 2,013 |
January 16, 2013 | https://www.sciencedaily.com/releases/2013/01/130116123013.htm | Leopards and tigers in India: New genetics research underscores importance of protecting forest corridors | As rapid economic expansion continues to shape the Asian landscape on which many species depend, time is running out for conservationists aiming to save wildlife such as tigers and leopards. Scientists at the Smithsonian Conservation Biology Institute have used genetic analysis to find that the natural forest corridors in India are essential to ensuring a future for these species. According to two studies recently published in two papers, these corridors are successfully connecting populations of tigers and leopards to ensure genetic diversity and gene flow. | The results of the study that focused on tigers were published in "This research provides crucial information about the need to maintain these vital veins to support tiger and leopard populations," said Sandeep Sharma, SCBI visiting scholar and lead author of the Ecology and Evolution paper. "These habitats and corridors in India are threatened by infrastructural developments and need to be conserved if we want to save these species for future generations."Habitat fragmentation can divide populations of species into isolated groups, which can lead to inbreeding and a genetic bottleneck that affects the long-term viability of the population. Scientists can determine the scope of such isolation by analyzing the extent to which groups of the same species from one range have become genetically distinct. The authors of the two papers used fecal samples to analyze the genetics of tiger and leopard populations in four reserves in central India: Satpura, Melghat, Pench and Kanha. The Kanha and Pench reserves and the Satpura and Melghat reserves are connected via forest corridors that tigers, leopards, humans and cattle share.The researchers found that both tiger and leopard populations in the reserves had maintained a high level of genetic diversity. Neither tigers nor leopards were genetically distinct, with one exception among the leopards, which the scientists hope to explain with additional research. The corridors appear to allow individuals to move between reserves, facilitating genetic exchange.However, the proliferation of roads, rail lines, mining, urbanization and other forms of development through the corridors jeopardize these species' ability to move between reserves. Several coal mines have been proposed in the forest corridor between the Satpura and Pench tiger reserves, as has the widening of a national highway (NH-7) and a broad-gauge railway line that cut across the corridor between the Kanha and Pench tiger reserves."By looking at two species, we were really able to illustrate the functionality of these corridors," said Trishna Dutta, SCBI visiting student and lead author of the Diversity and Distributions paper. "Conserving a whole landscape, rather than piecemeal protected areas, would ensure a better chance for the long-term persistence of these and other species."The Indian subcontinent contains the largest number of tiger conservation areas, which are home to 60 percent of the world's wild tigers. Leopard range has historically extended through most of sub-Saharan Africa, along parts of the North African coast, through central, south and southeast Asia and north to the Amur River valley in Russia.In addition to Sharma and Dutta, the papers' other SCBI authors are Jesús Maldonado, a research geneticist at SCBI's Center for Conservation and Evolutionary Genetics, and John Seidensticker, head of SCBI's Conservation Ecology Center. The other authors are Thomas Wood in the Department of Environmental Science and Policy at George Mason University and H.S. Panwar, former director of Project Tiger India and Wildlife Institute of India.The Smithsonian Conservation Biology Institute plays a key role in the Smithsonian's global efforts to understand and conserve species and train future generations of conservationists. Headquartered in Front Royal, Va., SCBI facilitates and promotes research programs based at Front Royal, the National Zoo in Washington, D.C., and at field research stations and training sites worldwide. | Genetically Modified | 2,013 |
January 15, 2013 | https://www.sciencedaily.com/releases/2013/01/130115111746.htm | Designer bacteria may lead to better vaccines | Researchers at The University of Texas at Austin have developed a menu of 61 new strains of genetically engineered bacteria that may improve the efficacy of vaccines for diseases such as flu, pertussis, cholera and HPV. | The strains of "For 70 years the only adjuvants being used were aluminum salts," said Stephen Trent, associate professor of biology in the College of Natural Sciences. "They worked, but we didn't fully understand why, and there were limitations. Then four years ago the first biological adjuvant was approved by the Food and Drug Administration. I think what we're doing is a step forward from that. It's going to allow us to design vaccines in a much more intentional way."Adjuvants were discovered in the early years of commercial vaccine production, when it was noticed that batches of vaccine that were accidentally contaminated often seemed to be more effective than those that were pure."They're called the 'dirty little secret' of immunology," said Trent. "If the vials were dirty, they elicited a better immune response."What researchers eventually realized was that they could produce a one-two punch by intentionally adding their own dirt (adjuvant) to the mix. The main ingredient of the vaccine, which was a killed or inactivated version of the bacteria or virus that the vaccine was meant to protect against, did what it was supposed to do. It "taught" the body's immune system to recognize it and produce antibodies in response to it.The adjuvant amplifies that response by triggering a more general alarm, which puts more agents of the immune system in circulation in the bloodstream, where they can then learn to recognize the key antigen. The result is an immune system more heavily armed to fight the virus or bacteria when it encounters it in the future.For about 70 years the adjuvant of choice, in nearly every vaccine worldwide, was an aluminum salt. Then in 2009, the FDA approved a new vaccine for human papillomavirus (HPV). It included a new kind of adjuvant that's a modified version of an endotoxin molecule.These molecules, which can be dangerous, appear on the cell surface of a wide range of bacteria. As a result, humans have evolved over millions of years to detect and respond to them quickly. They trigger an immediate red alert."In some of its forms an endotoxin can kill you," said Trent. "But the adjuvant, which is called MPL, is a very small, carefully modified piece of it, so it's able to trigger the immune response without overdoing it."What Trent and his colleagues have done is expand on that basic premise. Rather than just work with an inert piece of endotoxin, they've engineered "These 61 One form might work better with cholera vaccine, another with pertussis (whooping cough) and another with a future HIV vaccine. Trent, Needham and their colleagues should be able to fine-tune the adjuvants with increasing precision as more "I think we're at the dawn of a new age of vaccine design," said Trent. "For a long time vaccinology was really a trial-and-error field. It was a black box. We knew certain things worked. We knew certain vaccines had certain side effects. But we didn't entirely know why. Now that's changing."Trent said that an additional advantage of their system is that the "It makes possible a vaccine that provides protection from multiple pathogens at the same time," said Trent.Trent and his colleagues are working on a second round of designer "This is ready to go," said Trent. "I can't predict whether it will actually make it to the market. But it's very similar to the adjuvant that has already been approved, and my instinct is that if a company will undertake to do the trials, it will get approved. A company could call us tomorrow, we could send them a strain, and they could start working." | Genetically Modified | 2,013 |
January 10, 2013 | https://www.sciencedaily.com/releases/2013/01/130110111727.htm | Giant tobacco plants that stay young forever | Tobacco plants bloom when they are just a few months old -- and then they die. Now, researchers have located a genetic switch which can keep the plants young for years and which permits unbounded growth. In short, an ideal source of biomass. | The life of tobacco plants is short. They grow for around three to four months, followed by flowering and then die. Their size is also limited, with plants only growing to about one-and-a-half to two meters tall. Now, researchers at the Fraunhofer Institute for Molecular Biology and Applied Ecology IME in Münster have located the tobacco plant's very own fountain of youth, which means they can keep it forever young. The Münster-based researchers discovered a genetic switch which can prevent the plants from change blooming to flowering. This also averts the plants' early change demise to senescence -- and suppresses the factor that halts growth."The first of our tobacco plants is now almost eight years old but it still just keeps on growing and growing," says Professor Dirk Prüfer, head of the Department of Functional and Applied Genomics at the IME. "Although we regularly cut it, it's six-and-a-half meters tall. If our greenhouse were a bit higher, it would probably be even bigger. Its stem is already ten centimeters in diameter." Whereas in normal tobacco plants the leaves, which grow from the bottom of the stem, soon turn yellow and drop off, the IME plant's leaves stay healthy and green. This is why the scientists have christened their modified plant species "forever young."But what exactly do researchers do to give the plants eternal youth and make them capable of unbounded growth? "We modify the expression of a certain gene -- or rather, the information contained within it -- so that the plant's flowering is delayed," explains Prüfer. Researchers then insert the modified gene back into the plant using a bacterium. The role of the bacterium is to act as a sort of shuttle service for the modified gene.The principle is transferable and could be used on other kinds of plants; at the moment, the scientists are working also on potato plants on behalf of a Japanese chemical company. They use their knowledge to get crops to yield a far greater amount of biomass. In the case of potatoes, this means a great deal more starch."If we want to guarantee security of supply for foodstuffs and plant-based raw materials, the yield per hectare will have to double by 2050, claims the German Bioeconomy Council. This new technology brings us a great deal nearer to that target," reckons Prüfer. "However, our method is only likely to deliver success as long as the flowers of the plant in question play no significant role -- sugar beet, for instance. It would make no sense to use the technique on rapeseed." Preventing plants from flowering presents a significant advantage, in that no flowering means no production of seeds or pollen. As a result, plants have no way of reproducing, which means they cannot spread into the environment in an unplanned way.In the future, the researchers want to go further and be able to disable plants' growth limits using chemical mutagenesis as well -- that is to say, using normal growing techniques. This process involves using chemical additives to bring about changes in a seed's DNA sequence. The advantage is that a plant grown in this way would no longer be genetically modified but simply a plant grown using standard techniques. "But in order to be able to do that, we first need to gain a better understanding of the deregulation of genes," says Prüfer, who hopes cultivation experiments might begin next year. Then perhaps normal plants will be in a position to grow tall, too. | Genetically Modified | 2,013 |
January 10, 2013 | https://www.sciencedaily.com/releases/2013/01/130110075358.htm | Research revisiting the safety of GM weevil-resistant peas in mice contradicts previous risk assessment findings | Researchers at the Medical University of Vienna have conducted feeding trials with mice to investigate the allergenicity of genetically modified (GM) weevil-resistant peas. Development of the peas was discontinued in 2005 when a risk assessment conducted by the CSIRO and Australian National University showed negative reactions in mice to the peas (Prescott et al 2005). | Field peas are an important rotation crop, which can be devastated by pea weevil (The MedUni Vienna-team investigated immune responses in mice fed several varieties of beans, non-transgenic peas and the transgenic peas, expressing the bean or the transgenic versions of the α-amylase inhibitor. The mice showed similar levels of immune response no matter which food they consumed.Dr. Michelle Epstein, the lead researcher said, "We observed that the immune response in mice was the same no matter whether the inhibitor came from beans, where it naturally occurs, or from peas genetically modified to express the inhibitor and even in non-transgenic peas." "These results demonstrate that αAI transgenic peas are no more allergenic than beans or non-transgenic peas in mice" Dr. Epstein added.The Prescott study is regularly cited by those on both sides of the GM debate as an example of either the inherent dangers of genetically modified foods or the effectiveness of pre-market studies in identifying potential risk factors. Rodent studies for genetically modified organism (GMO) safety have recently been in the news. Seralini et al. showed untoward effects in rats fed GM corn but these studies were fraught with problems and add to the controversy of using rodents to study GMO safety (see EFSA report)."The study is important because it illustrates the significance of repeating experiments in independent laboratories" Dr. Epstein said. "It is also vital that investigators are aware of potential unexpected crossreactive allergic responses upon the consumption of plant products, as we found in the non-transgenic peas." Dr. Epstein questions the utility of rodents for evaluating biotech crops and points out that the MUV results highlight the importance of a careful case-by-case evaluation of GM crops, and the role science can play in decision-making around the introduction of GMOs into the food system.This research was conducted at the Medical University of Vienna as part of the European Commission Framework 7-funded GMSAFOOD project. | Genetically Modified | 2,013 |
January 9, 2013 | https://www.sciencedaily.com/releases/2013/01/130109160932.htm | Engineering alternative fuel with cyanobacteria | Sandia National Laboratories Truman Fellow Anne Ruffing has engineered two strains of cyanobacteria to produce free fatty acids, a precursor to liquid fuels, but she has also found that the process cuts the bacteria's production potential. | Micro-algal fuels might be one way to reduce the nation's dependence on foreign energy. Such fuels would be renewable since they are powered by sunlight. They also could reduce carbon dioxide emissions since they use photosynthesis, and they could create jobs in a new industry. President Barack Obama, speaking in February at the University of Miami, advocated for investments in algae fuel development, saying they could replace up to 17 percent of the oil the United States now imports for transportation."Even if algae are not the end-term solution, I think they can contribute to getting us there," Ruffing said. "Regardless of however you look at fossil fuels, they're eventually going to run out. We have to start looking to the future now and doing research that we'll need when the time comes."She has been studying the direct conversion of carbon dioxide into biofuels by photosynthetic organisms under a three-year Truman Fellowship that ends in January. She presented her project at a poster session in August and published her work on one strain, "Physiological Effects of Free Fatty Acid Production in Genetically Engineered Synechococcus elongatus PCC 7942," as the cover article in the September 2012 issue of Ruffing considers her studies as proof-of-concept work that demonstrates engineering cyanobacteria for free fatty acid (FFA) production and excretion. She wants to identify the best hydrocarbon targets for fuel production and the best model strain for genetic engineering, as well as gene targets to improve FFA production.She is using cyanobacteria -- blue-green algae -- because they are easier to genetically manipulate than eukaryotic algae, the natural "oil"-producing photosynthetic microorganisms more commonly used for algal biofuels, and because cyanobacteria can be engineered to create a variety of target fuels. Genetically engineered cyanobacteria excrete FFA and allow fuel to be collected without harvesting the cyanobacteria. This lowers the requirement for nitrogen and phosphate and reduces costs.But current yields from engineered strains are too low for large-scale production.Ruffing favors cyanobacteria because fuel from engineered cyanobacteria is excreted outside the cell, in contrast to eukaryotic algae, in which fuel production occurs inside the cell.In general, this is how the process works: Eukaryotic algae grow in a pond to the density needed, then producers must get rid of the water, collect the cells and break them open to get the fuel precursor inside. This precursor is isolated and purified, then chemically converted into biodiesel. Cyanobacteria excrete the fuel precursor outside the cell, so a separation process can remove the product without killing the cells. That eliminates the need to grow a new batch of algae each time, saving on nitrogen and phosphate.While other research efforts have focused on metabolic engineering strategies to boost production, Ruffing wants to identify what physiological effects limit cell growth and FFA synthesis."You can't really hope to continue to engineer it to produce more of the fatty acids until you address these unforeseen effects," she said. "As much as you want to do the applied side of things, creating the strain, you can't get away from the fundamental biology that's necessary in order to do that."Much of our fundamental understanding of photosynthesis comes from cyanobacteria, but it's only been in the past decade or so, with advances in gene manipulation and recombinant DNA technology, that they've been considered for fuel production, Ruffing said.The strains she engineered for FFA production show reduced photosynthetic yields, degradation of chlorophyll-a and changes in light-harvesting pigments, Ruffing said. She saw some cell death and lower growth rates overall, and suspects the toxicity of unsaturated FFA and changes in membrane composition are responsible.Now she's looking at what genes are changing when cyanobacteria produce fatty acids. She's creating mutants by knocking out certain genes or introducing or overexpressing genes to see how that affects the cell and fatty acid production."So I'm engineering the cell, then I'm trying to learn from the cell how to work with the cell to produce the fuel instead of trying to force it to produce something it doesn't want to produce," she said.She's producing FFA from Synechococcus elongatus PCC 7942 and Synechococcus sp. PCC 7002, chosen as so-called model organisms that have been studied for several decades and for which tools exist to manipulate their genes. She also is working with the two strains and a third, Synechocystis sp. PCC 6803, for biofuel toxicity screening.Ruffing hopes to continue working on strain development after the fellowship ends."It is possible that there's a natural strain out there that could be a better option, so this is still pretty early research," she said. "There's a lot of exploration to do." | Genetically Modified | 2,013 |
January 3, 2013 | https://www.sciencedaily.com/releases/2013/01/130103143205.htm | Editing genome with high precision: New method to insert multiple genes in specific locations, delete defective genes | Researchers at MIT, the Broad Institute and Rockefeller University have developed a new technique for precisely altering the genomes of living cells by adding or deleting genes. The researchers say the technology could offer an easy-to-use, less-expensive way to engineer organisms that produce biofuels; to design animal models to study human disease; and to develop new therapies, among other potential applications. | To create their new genome-editing technique, the researchers modified a set of bacterial proteins that normally defend against viral invaders. Using this system, scientists can alter several genome sites simultaneously and can achieve much greater control over where new genes are inserted, says Feng Zhang, an assistant professor of brain and cognitive sciences at MIT and leader of the research team."Anything that requires engineering of an organism to put in new genes or to modify what's in the genome will be able to benefit from this," says Zhang, who is a core member of the Broad Institute and MIT's McGovern Institute for Brain Research.Zhang and his colleagues describe the new technique in the Jan. 3 online edition of The first genetically altered mice were created in the 1980s by adding small pieces of DNA to mouse embryonic cells. This method is now widely used to create transgenic mice for the study of human disease, but, because it inserts DNA randomly in the genome, researchers can't target the newly delivered genes to replace existing ones.In recent years, scientists have sought more precise ways to edit the genome. One such method, known as homologous recombination, involves delivering a piece of DNA that includes the gene of interest flanked by sequences that match the genome region where the gene is to be inserted. However, this technique's success rate is very low because the natural recombination process is rare in normal cells.More recently, biologists discovered that they could improve the efficiency of this process by adding enzymes called nucleases, which can cut DNA. Zinc fingers are commonly used to deliver the nuclease to a specific location, but zinc finger arrays can't target every possible sequence of DNA, limiting their usefulness. Furthermore, assembling the proteins is a labor-intensive and expensive process.Complexes known as transcription activator-like effector nucleases (TALENs) can also cut the genome in specific locations, but these complexes can also be expensive and difficult to assemble.The new system is much more user-friendly, Zhang says. Making use of naturally occurring bacterial protein-RNA systems that recognize and snip viral DNA, the researchers can create DNA-editing complexes that include a nuclease called Cas9 bound to short RNA sequences. These sequences are designed to target specific locations in the genome; when they encounter a match, Cas9 cuts the DNA.This approach can be used either to disrupt the function of a gene or to replace it with a new one. To replace the gene, the researchers must also add a DNA template for the new gene, which would be copied into the genome after the DNA is cut.Each of the RNA segments can target a different sequence. "That's the beauty of this -- you can easily program a nuclease to target one or more positions in the genome," Zhang says.The method is also very precise -- if there is a single base-pair difference between the RNA targeting sequence and the genome sequence, Cas9 is not activated. This is not the case for zinc fingers or TALEN. The new system also appears to be more efficient than TALEN, and much less expensive.The new system "is a significant advancement in the field of genome editing and, in its first iteration, already appears comparable in efficiency to what zinc finger nucleases and TALENs have to offer," says Aron Geurts, an associate professor of physiology at the Medical College of Wisconsin. "Deciphering the ever-increasing data emerging on genetic variation as it relates to human health and disease will require this type of scalable and precise genome editing in model systems."The research team has deposited the necessary genetic components with a nonprofit called Addgene, making the components widely available to other researchers who want to use the system. The researchers have also created a website with tips and tools for using this new technique.Among other possible applications, this system could be used to design new therapies for diseases such as Huntington's disease, which appears to be caused by a single abnormal gene. Clinical trials that use zinc finger nucleases to disable genes are now under way, and the new technology could offer a more efficient alternative.The system might also be useful for treating HIV by removing patients' lymphocytes and mutating the CCR5 receptor, through which the virus enters cells. After being put back in the patient, such cells would resist infection.This approach could also make it easier to study human disease by inducing specific mutations in human stem cells. "Using this genome editing system, you can very systematically put in individual mutations and differentiate the stem cells into neurons or cardiomyocytes and see how the mutations alter the biology of the cells," Zhang says.In the The research was funded by the National Institute of Mental Health; the W.M. Keck Foundation; the McKnight Foundation; the Bill & Melinda Gates Foundation; the Damon Runyon Cancer Research Foundation; the Searle Scholars Program; and philanthropic support from MIT alumni Mike Boylan and Bob Metcalfe, as well as the newscaster Jane Pauley. | Genetically Modified | 2,013 |
December 20, 2012 | https://www.sciencedaily.com/releases/2012/12/121220143936.htm | Can observations of a hardy weed help feed the world? | As the human population increases, so too do the demands and stresses on agriculture. In the January 2013 issue of | In the article, Dr. Assmann describes how human population growth presents new challenges to twenty-first-century agriculture, especially since such abiotic stresses as climate change and poor-quality soils can disrupt the ability of many crops to flourish and provide sufficient calories, nutrients, and other resources. According to the U.N.'s Food and Agriculture Organization, Earth's population will reach nine billion people by the year 2050. To meet the needs of this population, Dr. Assmann says, plant biologists must study how and why some plants are heartier and more capable than others of tolerating these stresses.Dr. Assmann's focus is on a small flowering plant, a distant cousin of cabbage and canola that can be found growing wild across much of the globe. She explains that this species, "Ideally, if we can understand better the genetic diversity of this species, we can begin to explore the possibility of related biotechnological manipulations within crop species," Dr. Assmann says. "Here we have a great opportunity to harness the genetic variation in The | Genetically Modified | 2,012 |
December 20, 2012 | https://www.sciencedaily.com/releases/2012/12/121220143750.htm | Production of 5-aminovaleric and glutaric acid by metabolically engineered microorganism | We use many different types of chemicals and plastics for the convenience of our everyday life. The current sources of these materials are provided from petrochemical industry, using fossil oil as a raw material. Due to our increased concerns on the environmental problems and fossil resource availability, there has been much interest in producing those chemicals and materials from renewable non-food biomass through biorefineries. | For the development of biorefinery process, microorganisms have successfully been employed as the key biocatalysts to produce a wide range of chemicals, plastics, and fuels from renewable resources. However, the natural microorganisms without modification are not suitable for the efficient production of target products at industrial scale due to their poor metabolic performance. Thus, metabolic capacities of microorganisms have been improved to efficiently produce desired products, the performance of which is suitable for industrial production of such products. Optimization of microorganism for the efficient production of target bioproducts has been achieved by systems metabolic engineering, which allows metabolic engineering at the systems-level.5-aminovalic acid (5AVA) is the precursor of valerolactam, a potential building block for producing nylon 5, and can potentially be used as a C5 platform chemical for synthesizing 5-hydroxyvaleric acid, glutaric acid, and 1,5-pentanediol. It has been reported that a small amount of 5AVA is accumulated in In the paper published in Firstly, they constructed metabolic pathway to produce 5-aminovaleric acid (5AVA) using L-lysine as a direct precursor by employing two enzymes lysine 2-monooxygenase (DavB) and delta-aminovaleramidase (DavA). Secondly, metabolic pathway for the further conversion of 5AVA into glutaric acid was constructed by employing two more enzymes 5AVA aminotransferase (GabT) and glutarate semialdehyde dehydrogenase (GabD). Recombinant | Genetically Modified | 2,012 |
December 19, 2012 | https://www.sciencedaily.com/releases/2012/12/121219142303.htm | Soybeans a source of valuable chemical | The humble soybean could become an inexpensive new source of a widely used chemical for plastics, textiles, drugs, solvents and as a food additive. | Succinic acid, traditionally drawn from petroleum, is one focus of research by Rice chemists George Bennett and Ka-Yiu San. In 2004, the Department of Energy named succinic acid one of 12 "platform" chemicals that could be produced from sugars by biological means and turned into high-value materials.Several years ago, Rice patented a process by Bennett and San for the bio-based production of succinic acid that employed genetically modified The new succinate process developed by Bennett, San and Chandresh Thakker and reported recently in Bioresource Technology promises to make even better use of a cheap and plentiful feedstock, primarily the indigestible parts of the soybean."We are trying to find a cheaper, renewable raw material to start with so the end product will be more profitable," said Thakker, a research scientist in the Bennett lab at Rice's BioScience Research Collaborative and lead author of the study. "The challenge has been to make this biomass process cost-competitive with the petrochemical methods people have been using for many years."Bennett feels they have done that with soybean-derived feedstock as an inexpensive source of the carbon that microorganisms digest to produce the desired chemical via fermentation. "A lot of people use plant oils for cooking -- corn or soybean or canola -- instead of lard, as they did in the old days," he said. "The oils are among the main products of these seeds. Another product is protein, which is used as a high-quality food."What's left over is indigestible fiber and small carbohydrates," said Bennett, Rice's E. Dell Butcher Professor of Biochemistry and Cell Biology. "It's used in small amounts in certain animal feeds, but overall it's a very low-value material."The Rice researchers are changing that with the help of Expanding on their success in producing succinic acid from glucose, the new microbes are engineered to metabolize a variety of sugars found in soybean meal. The theoretical ideal is a 1:1 ratio of feedstock (the extracted sugars) to product, which they feel is achievable by industry. In the lab, under less controlled conditions, they still found the process highly efficient. "We're demonstrating a very high yield," Thakker said. "We're achieving in a flask a non-optimized formation of succinate that is close to the theoretical goal."Bennett said his lab has been looking at soybeans for nearly three years. "We're always interested in low-cost feedstock," he said. "We were able to get a connection with a soybean group that is very interested in technologies to make better and more profitable use of their crop."There's a fair amount of oilseed residuals available, including cottonseed carbohydrates, that are not used for any high-value product, and we're in the space of microbial engineering to enable these sorts of materials to be used in a good way," he said. | Genetically Modified | 2,012 |
December 18, 2012 | https://www.sciencedaily.com/releases/2012/12/121218081622.htm | Genetic markers for the conservation of wild herbivores in the Serengeti ecosystem in Tanzania | Tanzania is one of the few African countries with a diversity of wildlife species and a network of protected areas for these animals. The mapping of genetic variations in wild animals can help to improve wildlife management in the country. | A large number of tourists visit Tanzania in order to see African wild animals in their authentic environment. Researchers from many countries are also interested in studying the Tanzanian ecosystems. The greatest challenge facing the country is the sustainable conservation of biological diversity while at the same time promoting the development of infrastructure and welfare for the human populations living around the protected areas. Even though the number of wild species is seen to be on the decrease, especially large herbivores, Tanzania is striving to maintain its biological diversity. An important part of this work involves acquiring knowledge about the genetics of the species of wild animals in the region.As a result of his doctoral research, Eblate Ernest Mjingo has developed genetic tools, so-called microsatellites, for use in genetic studies of wild herbivores in the Serengeti ecosystem. The microsatellites he developed were then used to map the genetic structure of two important species in the ecosystem. One was the African buffalo, with a view to uncovering the possible effects human activity has on its genetics; the other was the wildebeest, where Mjingo studied the genetic differentiation between migrating and non-migrating populations.Mjingo's research reveals that populations of African buffalo living in the Serengeti ecosystem differ genetically. The population in Ngorongoro is different from the populations in the Serengeti National Park and the Maswa Game Reserve. This is because the habitats in the protected areas are separated from each other due to increased human activity. An increasing number of settlements and small-scale nomadic agriculture around Ngorongoro have created a barrier for the natural flow of genes throughout the Serengeti ecosystem. In order to conserve genetic diversity, it is important that the gene flow between the different areas is maintained.The results of Mjingo's research also show that migrating and non-migrating populations of wildebeest in the Serengeti ecosystem are genetically structured. He indicates that the wildebeest populations in Serengeti have adapted genetically to local environmental conditions and that different sub-populations have developed different strategies for survival. His thesis suggests that non-migrating animals should be kept as separate populations as these can act as a buffer for the genetic diversity and maintain the development potential of the species within the ecosystem.The results of Mjingo's PhD research project have provided us with new knowledge about genetic variation in large herbivores in Serengeti and with a platform for further research into the protection of wild ruminants, not only in Tanzania, but also in the whole sub-saharan region.Eblate Ernest Mjingo defended his doctoral research on 7 | Genetically Modified | 2,012 |
December 14, 2012 | https://www.sciencedaily.com/releases/2012/12/121214191518.htm | Drug used to treat HIV might defuse deadly staph infections | A new study by NYU School of Medicine researchers suggests that an existing HIV drug called maraviroc could be a potential therapy for | "What are the chances that a drug for HIV could possibly treat a virulent Staph infection?" asks Victor J. Torres, PhD, assistant professor of microbiology, and senior author of the study. "These findings are the result of a fantastic collaboration that we hope will result in significant clinical benefit." Staph causes toxic shock syndrome, pneumonia, and food poisoning, among other illnesses, and is becoming increasingly resistant to antibiotics.The discovery arose from a serendipitous finding that was a part of a collaborative study between Dr. Torres, a bacteriologist, and immunologist Derya Unutmaz, MD, associate professor of microbiology and pathology and medicine, whose laboratories are adjacent to each other.They focused on a receptor called CCR5 that dots the surface of immune T cells, macrophages, and dendritic cells. Sixteen years ago, researchers at NYU School of Medicine discovered that CCR5 is the receptor HIV uses to gain entry into T cells in order to replicate, spread, and cause an infection that can progress into AIDS.That same receptor has now been found to be critical to the ability of certain strains of Staph to specifically target and kill cells with CCR5, which orchestrate an immune response against the bacteria. The scientists discovered that one of the toxins the bacterium releases, called LukED, latches on to CCR5 and subsequently punches holes through the membrane of immune cells, causing them to rapidly die. The LukED toxin belongs to a family of proteins called leukotoxins, encoded and produced by Staph to fight off the immune system's defenses.This discovery was made after Dr. Torres asked Dr. Unutmaz and fellow HIV researcher Nathaniel Landau, PhD, professor of microbiology, if he might use some of the human immune cells they had collected over the course of their HIV studies. The laboratories of all three scientists are adjacent to each other. Dr. Torres was trying to find out which immune cells were affected by different leukotoxins. Dr. Unutmaz gave him a T cell line, which they were using for their HIV infection studies and had previously engineered to express CCR5, to test the effects of these toxins."Within one hour flat, T cells with CCR5 all died when exposed to LukED" says Dr. Torres, whereas a similar T cell line that lacked the receptor was completely resistant to the toxin's effects. This observation quickly led to another set of experiments to determine that the LukED toxin was indeed interacting with the receptor and that its presence on the cell surface was necessary for the toxin to kill the cells.The investigators then treated cells with CCR5 with maraviroc, a drug on the market that binds to CCR5 and blocks HIV infection, and then exposed the cells to the Staph toxin. The result, the scientists say, was astonishing. "It was remarkable. Maraviroc completely blocked the toxic effects of this leukotoxin at doses similar to those used to inhibit HIV infection" Dr. Unutmaz says."The goal in blocking the toxin with maraviroc or similar agents is to give the upper hand to the immune system to better control the infection," Dr. Torres adds. The researchers further corroborated the critical role of CCR5 in Staph infections using a mouse model. When they infected mice susceptible to Staph infection with strains that contain the LukED toxin, almost all the mice died. However, mice that were genetically engineered to lack CCR5 on their cells survived this lethal Staph infection.Based on these findings, the investigators hope that future human clinical trials will determine whether drugs that block CCR5, such as maraviroc, could help the immune system to control the infection and potentially save lives.Other NYU School of Medicine researchers contributing to the study are Francis Alonzo III, PhD, Lina Kozhaya, Stephen A. Rawlings, Tamara Reyes-Robles, Ashley L. DuMont, and David G. Myszka, PhD.The study was funded by grants from the National Institutes of Health, the NYU School of Medicine Development Funds, and an American Heart Association Scientist Development Grant. | Genetically Modified | 2,012 |
December 13, 2012 | https://www.sciencedaily.com/releases/2012/12/121213121750.htm | New study brings long-sought vaccines for deadly parasite closer to reality | One major cause of illness from food-borne diseases is the parasite | To fight off pathogens, the immune system relies on Toll-like receptors (TLRs) -- a class of proteins that recognize microbes and activate immune responses. The important role of TLR11 in recognizing the In the new study, Ghosh, Sher, and their collaborators focused on the previously uncharacterized TLR12 because it is closely related to TLR11 and physically interacts with that receptor, suggesting that the two might work together to mount immune responses. When they genetically engineered mice to lack TLR12, they found that immune cells could not recognize or protect against "Prior to this study, TLR12 had no known function in the immune system, and it was not known what pathogen this receptor recognized," Ghosh says. "We have demonstrated that TLR12 is essential for resistance to Because TLR12 also recognized another related parasite, the findings could have broad clinical implications. "By investigating how immune cells expressing TLR12 organize the immune response against | Genetically Modified | 2,012 |
December 10, 2012 | https://www.sciencedaily.com/releases/2012/12/121210160846.htm | Biologists engineer algae to make complex anti-cancer 'designer' drug | Biologists at UC San Diego have succeeded in genetically engineering algae to produce a complex and expensive human therapeutic drug used to treat cancer. | Their achievement, detailed in a paper in this week's early online issue of "Because we can make the exact same drug in algae, we have the opportunity to drive down the price down dramatically," said Stephen Mayfield, a professor of biology at UC San Diego and director of the San Diego Center for Algae Biotechnology or SD-CAB, a consortium of research institutions that is also working to develop new biofuels from algae.Their method could even be used to make novel complex designer drugs that can't be produced in any other systems--drugs that could be used to treat cancer or other human diseases in new ways."You can't make these drugs in bacteria, because bacteria are incapable of folding these proteins into these complex, three-dimensional shapes," said Mayfield. "And you can't make these proteins in mammalian cells because the toxin would kill them."The advance is the culmination of seven years of work in Mayfield's laboratory to demonstrate that Mayfield and his colleagues achieved their first breakthrough five years ago when they demonstrated they could produce a mammalian serum amyloid protein in algae. The following year, they succeeded in getting algae to produce a human antibody protein. In 2010, they demonstrated that more complex proteins -- human therapeutic drugs, such as human vascular endothelial growth factor, or VEGF, used to treat patients suffering from pulmonary emphysema -- could be produced in algae.Then in May of this year, Mayfield's group working with another team headed by Joseph Vinetz from UC San Diego's School of Medicine, engineered algae to produce an even more complex protein -- a new kind of vaccine that, preliminary experiments suggest, could protect billions of people from malaria, one of the world's most prevalent and debilitating diseases."What the development of the malarial vaccine showed us was that algae could produce proteins that were really complex structures, containing lots of disulfide bonds that would still fold into the correct three-dimensional structures," said Mayfield. "Antibodies were the first sophisticated proteins we made. But the malarial vaccine is complex, with disulfide bonds that are pretty unusual. So once we made that, we were convinced we could make just about anything in algae."In their latest development, the scientists genetically engineered algae to produce a complex, three-dimensional protein with two "domains" -- one of which contains an antibody, which can home in on and attach to a cancer cell and another domain that contains a toxin that kills the bound cancer cells. Such "fusion proteins" are presently created by pharmaceutical companies in a complex, two-step process by first developing the antibody domain in a Chinese hamster, or CHO, cell. The antibody is purified, then chemically attached to a toxin outside of the cell. Then the final protein is re-purified."We have a two-fold advantage over that process," said Mayfield. "First, we make this as a single protein with the antibody and toxin domains fused together in a single gene, so we only have to purify it one time. And second, because we make this in algae rather than CHO cells, we get an enormous cost advantage on the production of the protein."The fusion protein the researchers in his laboratory produced from algae is identical to one that is under development by pharmaceutical companies with a proposed cost of more than $100,000. This same protein could be produced in algae for a fraction of that price, they report in their paper. And the UCSD researchers -- Miller Tran, Christina Van, Dan Barrera and Jack Bui, at the UC San Diego Medical School -- confirmed that the compound worked like the more expensive treatment: it homed in on cancer cells and inhibited the development of tumors in laboratory mice.Mayfield said such a fusion protein could not have been produced in a mammalian CHO cell, because the toxin would have killed it. But because the protein was produced in the algae's chloroplasts -- the part of algal and plant cells where photosynthesis takes place -- it did not kill the algae."The protein was sequestered inside the chloroplast," Mayfield said. "And the chloroplast has different proteins from the rest of the cell, and these are not affected by the toxin. If the protein we made were to leak out of the chloroplast, it would have killed the cell. So it's amazing to think that not one molecule leaked out of the chloroplasts. There are literally thousands of copies of that protein inside the chloroplasts and not one of them leaked out."Mayfield said producing this particular fusion protein was fairly straightforward because it involved fusing two domains -- one to recognize and bind to cancer cells and another to kill them. But in the future, he suspects this same method could be used to engineer algae to produce more complex proteins with multiple domains."Can we string together four or five domains and produce a designer protein in algae with multiple functions that doesn't exist in nature? I think we can?" he added. "Suppose I want to couple a receptor protein with a series of activator proteins so that I could stimulate bone production or the production of neurons? At some point you can start thinking about medicine the same way we think about assembling a computer, combining different modules with specific purposes. We can produce a protein that has one domain that targets the kind of cell you want to impact, and another domain that specifies what you want the cell to do."The research project was supported by grants from the National Science Foundation and The Skaggs Family Foundation. | Genetically Modified | 2,012 |
December 3, 2012 | https://www.sciencedaily.com/releases/2012/12/121203150014.htm | Arthritis research: Mouse model of diffuse idiopathic skeletal hyperostosis discovered | Researchers at Western University have made a breakthrough that could lead to a better understanding of a common form of arthritis that, until now, has eluded scientists. | According to The Arthritis Society, the second most common form of arthritis after osteoarthritis is "diffuse idiopathic skeletal hyperostosis" or DISH. It affects between six and 12 percent of North Americans, usually people older than 50. DISH is classified as a form of degenerative arthritis and is characterized by the formation of excessive mineral deposits along the sides of the vertebrae in the neck and back. Symptoms of DISH include spine pain and stiffness and in advanced cases, difficulty swallowing and damage to spinal nerves. The cause of DISH is unknown and there are no specific treatments.Now researchers at Western University's Bone and Joint Initiative, with collaborator Doo-Sup Choi at the Mayo Clinic in Rochester, Minnesota have discovered the first-ever mouse model of this disease. The research is published online in the "This model will allow us for the first time to uncover the mechanisms underlying DISH and related disorders. Knowledge of these mechanisms will ultimately allow us to test novel pharmacological treatments to reverse or slow the development of DISH in humans," says corresponding author Cheryle Séguin of the Skeletal Biology Laboratories and the Department of Physiology and Pharmacology at Western's Schulich School of Medicine & Dentistry.Graduate student Derek Bone, working under the supervision of pharmacologist James Hammond, was studying mice that had been genetically modified to lack a specific membrane protein that transports adenosine when he noticed that these mice developed abnormal calcification (mineralization) of spinal structures.Changes in the backbone of these mice were characterized by an interdisciplinary team which included: Sumeeta Warraich, Diana Quinonez, Hisataka Ii, Maria Drangova, David Holdsworth and Jeff Dixon. Their findings established that spinal mineralization in these mice resembles DISH in humans and point to a role for adenosine in causing abnormal mineralization in DISH. | Genetically Modified | 2,012 |
November 29, 2012 | https://www.sciencedaily.com/releases/2012/11/121129173948.htm | First direct evidence linking TB infection in cattle to local badger populations | Transmission of tuberculosis between cattle and badgers has been tracked at a local scale for the first time, using a combination of bacterial whole-genome DNA sequencing and mathematical modelling. The findings highlight the potential for next-generation sequencing to be used to understand the impact of badgers on TB outbreaks in cows at the farm level. | The role of badgers in the transmission of bovine tuberculosis (bTB) among cattle remains controversial: the government's proposal to implement a widespread badger cull in England was recently delayed and has met with extensive criticism over its evidence base.Previous studies have used lower resolution genetic typing of bacteria and information observed during an outbreak to identify links between cattle and badgers. Until now, however, direct evidence of transmission of the bacteria between the two hosts at the farm scale has been lacking.In this study, researchers made use of advances in genetic technologies to sequence whole genomes of bacteria that had been isolated from 26 cows and four badgers from a group of neighbouring farms in Northern Ireland over a decade-long history of repeated bTB outbreaks. This approach enabled the team to retrospectively trace changes in the bacteria's DNA as it passed from animal to animal.The findings reveal that the bacteria isolated from badgers and cattle were extremely closely related, and indistinguishable bacterial types were often obtained from badgers and nearby cattle farms. Moreover, the bacteria isolated from the two species were more closely related to each other than they were to farms even a few kilometres away."This study provides the first direct evidence of the close relationship between tuberculosis infections in cows and local badgers, at a very local scale," explains Professor Rowland Kao, a Wellcome Trust Senior Research Fellow who led the study jointly conducted by the University of Glasgow and the Agri-Food and Biosciences Institute in Northern Ireland. "However, only with a larger study might we be able to quantify the extent and direction of transmission between cattle and badgers and reliably inform disease control policies."The mathematical models used in this study show that different herd outbreaks were usually characterised by genetically distinct groups of bacteria, while bacteria from within single outbreaks were usually closely related, highlighting the potential to use next-generation sequencing to track the spread of the bacteria from herd to herd.Bovine tuberculosis (bTB) is an important disease of both livestock and wildlife with severe impacts on animal health and subsequent economic consequences. Although the disease in cattle is caused by a different bacteria to human disease (Mycobacterium bovis rather than Mycobacterium tuberculosis), M. bovis is believed to have been a major historical contributor to human cases of TB worldwide and remains a health concern in both high- and low-income countries.The study is published November 29 in the journal | Genetically Modified | 2,012 |
November 26, 2012 | https://www.sciencedaily.com/releases/2012/11/121126142850.htm | Bioengineered marine algae expands environments where biofuels can be produced | Biologists at UC San Diego have demonstrated for the first time that marine algae can be just as capable as fresh water algae in producing biofuels. | The scientists genetically engineered marine algae to produce five different kinds of industrially important enzymes and say the same process they used could be employed to enhance the yield of petroleum-like compounds from these salt water algae. Their achievement is detailed in a paper published online in the current issue of the scientific journal The ability to genetically transform marine algae into a biofuel crop is important because it expands the kinds of environments in which algae can be conceivably grown for biofuels. Corn, for example, which is used to produce ethanol biofuel, requires prime farmland and lots of fresh water. But the UC San Diego study suggests that algal biofuels can be produced in the ocean or in the brackish water of tidelands or even on agricultural land on which crops can no longer be grown because of high salt content in the soil."What our research shows is that we can achieve in marine species exactly what we've already done in fresh water species," said Stephen Mayfield, a professor of biology at UC San Diego, who headed the research project. "There are about 10 million acres of land across the United States where crops can no longer be grown that could be used to produce algae for biofuels. Marine species of algae tend to tolerate a range of salt environments, but many fresh water species don't do the reverse. They don't tolerate any salt in the environment.""The algal community has worked on fresh water species of algae for 40 years," added Mayfield, who also directs the San Diego Center for Algae Biotechnology, or SD-CAB, a consortium of research institutions in the region working to make algal biofuels a viable transportation fuel in the future. "We know how to grow them, manipulate them genetically, express recombinant proteins -- all of the things required to make biofuels viable. It was always assumed that we could do the same thing in marine species, but there was always some debate in the community as to whether that could really be done."That debate came to a head last month when a National Academy of Sciences committee examining the future potential of algal biofuels for the U.S. Department of Energy published a report pointing out that the production of algal biofuels might be limited by fresh water because no published research study had demonstrated the feasibility of using engineered marine species of algae."But now we've done it," said Mayfield. "What this means is that you can use ocean water to grow the algae that will be used to produce biofuels. And once you can use ocean water, you are no longer limited by the constraints associated with fresh water. Ocean water is simply not a limited resource on this planet."The UC San Diego biologists focused their study on a marine species of alga, Dunaliella tertiolecta, which had been earlier targeted by scientists for potential biofuels production because of its high oil content and ability to grow rapidly under a wide range of salinity and acidic conditions. To demonstrate that it could be used in commercial biofuel production, they introduced five genes into the alga that produced five different kinds of enzymes that could be used in an industrial setting to not only convert biomass to fuel, but also increase nutrient availability in animal feed. Some of these enzymes, for example, came from a fungus that degrades plant material into simple sugars.The scientists said in their paper that "we hope to eventually determine whether whole algae, post-oil extraction, may be used as a feed additive to improve animal feeds. Animal feed is a relatively high volume market that may be able to benefit from algae-produced proteins as a feed additive."The UC San Diego biologists -- who included D. Ryan Georgianna, Michael Hannon, Marina Marcuschi, Alex Lewis, James Hyun -- collaborated on their project with three scientists from Sapphire Energy, Inc., a San Diego algal biotechnology company -- Shuiqin Wu, Kyle Botsch and Michael Mendez. Their research effort was funded by the Air Force Office of Scientific Research and the State of California Energy Commission. | Genetically Modified | 2,012 |
November 21, 2012 | https://www.sciencedaily.com/releases/2012/11/121121210107.htm | Bornean Elephant: Genomics helps with conservation | Studying the genetic variability of endangered species is becoming increasingly necessary for species conservation and monitoring. But, endangered species are difficult to observe and sample, and typically harbour very limited genetic diversity. Until now, the process of finding genetic markers was time consuming and quite expensive. These obstacles make the collection of genetic data from endangered animals a difficult task to fulfill. A research team led by Lounès Chikhi, group leader at the Instituto Gulbenkian de Ciência (IGC) and CNRS researcher (in Toulouse, France), has now contributed to change the odds when looking for diversity. | Taking advantage of cutting edge DNA sequencing methodology and the collaborations with the Sabah Wildlife Department in Malaysia, Rachel O'Neill's laboratory (University of Connecticut) and a private company (Floragenex), they were able to identify the genetic markers for the Bornean elephant, an endangered species, using blood from very few animals. The results showed that Bornean elephants have very low genetic variability that can impact on their survival to a threatened habitat, but that variable genetic markers can still be identified. The study now published in the journal The Bornean elephant is a unique subspecies of the Asian elephant, with a quite distinct morphology and behavior. They are generally smaller than other elephants, with straight tusks and a long tail. Currently, there are around 2000 individuals, located only in the North of Borneo. It remains unknown how this population of elephants evolved to become so different and why its distribution is so restricted.Despite being one of the highest priority populations for Asian elephant conservation, until now there were limited genetic tools available to study its genetic variability and none that had been specifically designed for this species. Now, in the work conducted by Reeta Sharma, a Post-Doctoral fellow in Lounès Chikhi's group, for the first time DNA sequences that characterize the genome of the Bornean elephants, called genetic markers, were identified. The research team used two different DNA sequencing technologies that are fast and increasingly cheaper. This kind of technology has been used for common laboratory species such as mice and fruit-flies, but they are only now starting to be used on endangered and "non-model" species.Until now, in order to determine whether the species still harboured sufficient genetic diversity it was necessary to look through huge regions of the genome, using classical genetics methodologies, or use markers developed for other species, with varying levels of success. This approach can become unsustainable for the endangered species, whose numbers have gone bellow a certain size for long time. The only study that previously had tried to analyse Bornean elephants, using genetic markers developed for other Asian elephants had found nearly no genetic diversity. The work now developed demonstrates that if the methodology can be applied to the Bornean elephant, it should be possible to find the needles we need, and not get stuck with the hay, i.e., to find variable genetic markers in many other species.The DNA analysis done resulted from blood samples collected only from seven Bornean elephants from the Lok Kawi Wildlife Park (Sabah, Malaysia) and from Chendra, the star elephant of Oregon zoo (Portland, USA). But, the research team is confident that these DNA sequencing methods can be used to type genetically other biological samples, such as hair or faeces, easier to obtain from wild animals, even though blood or tissue samples are still necessary to identify the markers during the first steps.Reeta Sharma, first author of this work, says: 'The methodology applied to identify the genetic markers for the Bornean elephant can be used in the future for studies on the genetic variability of other species or populations facing the risk of extinction.'The Bornean elephants live in an environment where natural habitats disappear quickly, due to oil palm plantations and populations get isolated from each other. Having access to variable genetic markers will be crucial to identify populations that are isolated and genetically depauperate, and monitor them in the future.The origin of these elephants in Borneo raises controversy that has been long discussed. The only study done on the basis of genetic data concluded that they had been present in Borneo for more than 300,000 years. This theory does not satisfy all researchers as there is lack of elephant fossils in Borneo to support it. Another theory is that the sultan of Java sent Javan elephants as a gift to the sultan of Sulu, who would have introduced them to Borneo.Lounes Chikhi suggests: 'The new genetic markers that we found may also allow us to unravel the mystery of the origin of these elephants in Borneo, and perhaps reconstruct part of their demographic history. This is very exciting '.This research was carried out at the IGC in collaboration with the Laboratoire Evolution et Diversité Biologique in Toulouse, and with the School of Biosciences, Cardiff University (UK), the Sabah Wildlife Department (Malaysia), the Danau Girang Field Centre (Malaysia), the Center for Applied Genetics and Technology, University of Connecticut (USA) and Floragenex, Inc. (USA). Research was funded mainly by Fundação para a Ciência e a Tecnologia (FCT), Portugal, and Laboratoire d'Excellence (LABEX), France. | Genetically Modified | 2,012 |
November 16, 2012 | https://www.sciencedaily.com/releases/2012/11/121116124646.htm | Clocks are ticking and climate is changing: Increasing plant productivity in a changing climate | Dartmouth plant biologist C. Robertson (Rob) McClung is not your typical clock-watcher. His clocks are internal, biological, and operate in circadian rhythms -- cycles based on a 24-hour period. Living organisms depend upon these clocks to keep pace with Earth's daily rotation and the recurring changes it imposes on the environment. These clocks allow the plant or animal to anticipate the changes and adapt to them by modifying its biology, behavior, and biochemistry. | "If you know that the sun is going to go down, and if you are a photosynthetic plant, you have to readjust your metabolism in order to make it through the night," says McClung, the Patricia F. and Williams B. Hale 1944 Professor in the Arts and Sciences.McClung uses the According to the National Institutes of Health, this member of the mustard family is the model organism for studies of the cellular and molecular biology of flowering plants. "Because plants are closely related, it is quite likely that knowledge derived from McClung sees internal clocks as increasingly important in the face of global climate change, and to agricultural productivity in particular. "In the context of climate change and the need to exploit increasingly marginal habitats, fuller understanding of clock mechanisms may offer strategies to improve crop productivity," says McClung. "We need to know how an organism measures time and how it uses that information to coordinate its physiology and behavior."Water is the landscape on which biological clocks and climate change intersect. Agriculture consumes the vast majority of our water, and warmer and dryer conditions are predicted for much of the agricultural land of the United States. This is based on our current understanding of the changes predicted to be associated with global warming, and in this scenario our aquatic resources will become increasingly scarce.Water is lost during the gas exchange that takes place in photosynthesis -- carbon dioxide in, oxygen out -- through small pores in the surface of leaves that periodically open and close under the control of a biological clock. Exercising control over this clock could be a means of conserving water. "We know that these little cells on the surface of the leaf are controlled by the clock," says McClung. "It could be that different clocks regulate it slightly differently, and we would like to find the best clock, fine-tune it, and perhaps optimize the ability to get COWater figures prominently in another aspect of plant physiology. Water moves up through the stem to the leaves, involving proteins called aquaporins. "There is a big family of genes that encode aquaporins, and in Together with colleagues in Wyoming, Wisconsin, and Missouri, McClung has been looking at another crop, In a related project, McClung will be working with soybeans, attempting to correlate circadian period length with latitude. "If we can understand the clock, we might then manipulate the clock in ways to achieve desired goals, including water use efficiency and better yield."McClung feels strongly that this sort of basic research has the potential to contribute in significant ways to food production increases. "Whether or not we achieve that increase or whether it allows us to fertilize a little less and so pollute a little less but maintain the same productivity level, anything in the net direction that is positive is going to help," he says. "We can't necessarily say exactly how it will help, but I think it's not unreasonable to think that this very basic research can have a real world impact, and one hopes it will.""We will need to genetically modify our plants to control our circadian biological clocks," says Professor Rob McClung. "Every domesticated plant and animal that we have today is already genetically modified. None of them are as they are found in nature. We have manipulated their genes by selective breeding and creating hybrids."To produce the corn we eat today, prehistoric farmers first had to find some variant that had a desirable trait, keep its seeds and plant them, repeating the process for countless generations to bring out that trait. That is selective breeding and it produced a plant whose genome was modified.To make a tomato plant resistant to a particular disease or pest, we might find some related pest-resistant species in the wild and cross it with our garden variety tomato to produce a hybrid. Successive crosses would preserve the "tomato-ness" while selectively retaining that little bit from the wild relative that resists tomato-eating bugs."Along with introducing the gene or set of genes encoding resistance, we may have also brought in a whole bunch of other ill-defined genes on either side," McClung says. "We don't know the extent of it. We don't know what else is in there. While some regard this as a 'natural' approach, the unknown genetic fellow travelers could be problematic or even dangerous."For more than 20 years, we have possessed the technology to precisely insert a single gene, making one change and only one change, producing what is known as recombinant DNA. "We are modifying genes in a much more informed way and precise way, targeting specific genes and manipulating those," he says."Nevertheless, there is vocal opposition to this practice, in spite of the fact that we have been doing it for decades and there is yet to be a single example of anything bad happening from that," says McClung. "It is a philosophical standpoint based on a lack of understanding. People don't understand the science and they come up with a lot of arguments against it."The dilemma rests on timing. Conventional breeding, though imprecise and unpredictable, is a workable but lengthy process. Recombinant DNA is fast. In a world beset by overpopulation, famine and global climate change, McClung questions whether we can really afford the time to wait. | Genetically Modified | 2,012 |
November 13, 2012 | https://www.sciencedaily.com/releases/2012/11/121113143656.htm | New type of bacterial protection found within cells: Novel immune system response to infections discovered | UC Irvine biologists have discovered that fats within cells store a class of proteins with potent antibacterial activity, revealing a previously unknown type of immune system response that targets and kills bacterial infections. | Steven Gross, UCI professor of developmental & cell biology, and colleagues identified this novel intercellular role of histone proteins in fruit flies, and it could herald a new approach to fighting bacterial growth within cells. The study appeared November 13 in "We found that these histone proteins have pan-antibacterial abilities and can have a wide-ranging effect," Gross said. "If we can discover how to manipulate the system to increase histone levels, we may one day have a new way to treat patients with bad bacterial infections."Histones exist in large numbers in most animal cells; their primary job is to help DNA strands fold into compact and robust structures inside the nucleus. Gross said there is some evidence that histones secreted from cells protect against bacteria living outside cells. However, many bacteria enter cells, where they can avoid the immune system and continue replicating.In principle, Gross said, histones could protect cells against such bacteria from the inside, but for many years this was thought unlikely because most histones are bound to DNA strands in the cell nucleus, whereas bacteria multiply in the cellular fluid outside the nucleus, called cytosol. Additionally, free histones can be extremely damaging to cells, so most species have developed mechanisms to detect and degrade free histones in the cytosol.In their study, Gross and colleagues demonstrate that histones bound to lipid (fat) droplets can protect cells against bacteria without causing any of the harm normally associated with the presence of free histones. In experiments with lipid droplets purified from Drosophila fruit fly embryos, they show that lipid-bound histones can be released to kill bacteria.The researchers injected similar numbers of bacteria into Drosophila embryos that contained lipid-bound histones and into embryos genetically modified to not contain them. They discovered that the histone-deficient flies were 14 times more likely to die of bacterial infections. Similar results were found in experiments on adult flies. Additional evidence suggested that histones might also protect mice against bacteria."Because numerous studies have now identified histones on lipid droplets in many different cells -- from humans as well as mice and flies -- it seems likely that this system may be quite general," Gross said. | Genetically Modified | 2,012 |
November 13, 2012 | https://www.sciencedaily.com/releases/2012/11/121113083546.htm | G proteins regulate remodeling of blood vessels | Max Planck researchers are investigating the signalling pathways via which the smooth muscle cells of blood vessels react to extracellular changes. | Blood vessels are extremely dynamic: depending on the external conditions, they can adapt their permeability for nutrients, their contractility, and even their shape. Unlike cardiac muscle cells, for example, the smooth muscle cells in blood vessels demonstrate a high degree of plasticity, so they can specialise or multiply as required, even repairing damage to the vessel wall. This vascular remodelling is evidently precisely regulated. Disruptions are extremely significant in conditions such as atherosclerosis or high blood pressure. At the Max Planck Institute for Heart and Lung Research in Bad Nauheim, scientists conducting research on genetically modified mice have discovered how external signals regulate vascular remodelling at cell level. This has created an entirely new understanding of regulation, which could pave the way for new approaches in the prevention and treatment of atherosclerosis and other vascular diseases.The walls of blood vessels consist of smooth muscle cells, elastic fibres, and endothelial cells, which line the interior surface of the vessel. The vessels change their permeability and contractility as required. If a blood vessel is damaged, existing smooth muscle cells can give rise to new specialised muscle cells to repair it. However, in the case of a vascular problem, this necessary and useful cell plasticity can have negative consequences. For example, if a coronary blood vessel is opened up with dilatation and stents via a catheter, muscle cell growth may cause it to narrow once again. In the common condition atherosclerosis or vascular calcification, too, remodelling processes lead to formation of the dreaded plaque. All these processes are regulated by hormones or neurotransmitters, some of which are released by cells and nerves in the vessel wall. Most of these vasoactive messengers work by binding to receptors, which in turn, once activated, bind to what are known as G proteins. These are situated on the inside of the cell membrane and relay the signal from there into the cell interior."There are two different families of G proteins which play a crucial role in vascular remodelling. They are called GIn order to investigate the signalling pathways and their regulation, Till Althoff, who headed the study, examined mice whose genes for the various G proteins he had specifically deactivated. Thus the researcher was able to show, for example, that in a mouse suffering from atherosclerosis and missing G"We see here clearly that in vascular remodelling the two signalling pathways work as antagonists," Offermanns explains. Which is only sensible, as it is the only way a system can balance cell growth and regression. In further tests, the scientists also demonstrated the steps required for the two pathways to achieve their objective and stimulate the genes in the cell interior responsible for generating specialised cells or for cell growth."Our results really do reveal a completely new picture of the regulation of vascular remodelling, also in pathological processes," says Offermanns. The researchers are therefore hopeful that new pharmacological approaches can be developed. Offermanns can well imagine, for example, that drugs could be used to modulate plasticity in cases of vascular diseases like atherosclerosis or after cardiological interventions. Now that the target structures in both signalling pathways have been identified, new possibilities are opening up. For instance, the pathway that promotes growth could be blocked and the stabilising pathway activated in order to slow down the remodelling process. "In animal models we are already investigating new therapeutic approaches to preventing atherosclerosis and suppressing cell growth in damaged vessels," reports Offermanns. | Genetically Modified | 2,012 |
November 6, 2012 | https://www.sciencedaily.com/releases/2012/11/121106201124.htm | Humans, chimpanzees and monkeys share DNA but not gene regulatory mechanisms | Humans share over 90% of their DNA with their primate cousins. The expression or activity patterns of genes differ across species in ways that help explain each species' distinct biology and behavior. | DNA factors that contribute to the differences were described on Nov. 6 at the American Society of Human Genetics 2012 meeting in a presentation by Yoav Gilad, Ph.D., associate professor of human genetics at the University of Chicago.Dr. Gilad reported that up to 40% of the differences in the expression or activity patterns of genes between humans, chimpanzees and rhesus monkeys can be explained by regulatory mechanisms that determine whether and how a gene's recipe for a protein is transcribed to the RNA molecule that carries the recipe instructions to the sites in cells where proteins are manufactured.In addition to improving scientific understanding of the uniqueness of humans, studies such as the investigation conducted by Dr. Gilad and colleagues could have relevance to human health and disease."Through inter-species' comparisons at the DNA sequence and expression levels, we hope to identify the genetic basis of human specific traits and in particular the genetic variations underlying the higher susceptibility to certain diseases such as malaria and cancer in humans than in non-human primates," said Dr. Gilad.Dr. Gilad and his colleagues studied gene expression in lymphoblastoid cell lines, laboratory cultures of immortalized white blood cells, from eight humans, eight chimpanzees and eight rhesus monkeys.They found that the distinct gene expression patterns of the three species can be explained by corresponding changes in genetic and epigenetic regulatory mechanisms that determine when and how a gene's DNA code is transcribed to a messenger RNA (mRNA) molecule.Dr. Gilad also determined that the epigenetics process known as histone modification also differs in the three species. The presence of histone marks during gene transcription indicates that the process is being prevented or modified."These data allowed us to identify both conserved and species-specific enhancer and repressor regulatory elements, as well as characterize similarities and differences across species in transcription factor binding to these regulatory elements," Dr. Gilad said.Among the similarities among the three species were the promoter regions of DNA that initiated transcription of a particular gene.In all three species, Dr. Gilad's lab found that transcription factor binding and histone modifications were identical in over 67% of regulatory elements in DNA segments that are regarded as promoter regions.The researchers presentation is titled, "Genome-wide comparison of genetic and epigenetic regulatory mechanisms in primates." | Genetically Modified | 2,012 |
November 5, 2012 | https://www.sciencedaily.com/releases/2012/11/121105151342.htm | New DNA vaccine technology poised to deliver safe and cost-effective disease protection | New and increasingly sophisticated vaccines are taking aim at a broad range of disease-causing pathogens, targeting them with greater effectiveness at lower cost and with improved measures to ensure safety. | To advance this quest, a research team led by Roy Curtiss, director of the Center for Infectious Diseases and Vaccinology, and Wei Kong, a research assistant professor, at Arizona State University's Biodesign Institute have taken a dramatic step forward, revealing the design of a universal platform for delivering highly potent DNA vaccines, by employing a cleverly re-engineered bacterium to speed delivery to host cells in the vaccine recipient."The technology that we're describing in this paper can be used to develop a vaccine against any virus, any parasite, any fungus, whereas this was never possible before the development of recombinant attenuated bacterial strains like those produced in our lab," Curtiss says.The experimental vaccine described in the new research demonstrated complete protection from influenza in mice, but Wei Kong, the leading author of the new study stresses that the innovative technique could be applied to the rapid manufacture of effective vaccines against virtually any infectious invader at dramatically reduced cost and without risk to either those vaccinated or the wider public."By delivering the DNA vaccine using a recombinant attenuated bacterium, we can get 10,000-100,000 doses per liter of culture," Kong says, an improvement of 3-4 orders of magnitude over use of the naked plasmid DNA, which must be painstakingly isolated from bacteria before injection.The group's research results appear in the online Early Edition (EE) of the Designing a vaccine that is both safe and effective presents a kind of Catch-22 for researchers. Live pathogenic strains typically generate a robust immune response, mimicking natural infection, but many challenges exist in terms of ensuring such strains do not cause illness or escape into the environment, where they have the potential to remain viable. Killed pathogen strains or vaccines produced from pathogen subunits sacrifice some of their immunogenic effectiveness for enhanced safety, and may require subsequent booster doses to ensure continued effectiveness.The Curtiss team has worked to combine safety and effectiveness in orally administered vaccines that can be produced at a fraction of the cost of traditional methods. To do this, they have pioneered techniques using Salmonella -- the notorious agent associated with food-borne illness -- as a cargo vessel to deliver a suite of disease antigens to the recipient. The result has been the development and ongoing refinement of so-called RASVs (for recombinant attenuated Salmonella vaccines), capable of provoking an intense, system-wide immune response and conferring effective immunity.One of the key innovations developed earlier by Wei Kong and other members of the Curtiss group, is a specialized Salmonella strain that can be timed to self-destruct in the body once it has carried out its immunization duties. To create this strain, the researchers modified the bacterium in such a way that it can only survive on a non-naturally occurring form of sugar. Once the Salmonella cells exhaust their store of specialized sugar, supplied to them as part of the vaccine, they are unable to maintain the integrity of their cell walls and they essentially implode. "This crucial safety feature ensures that Salmonella are unable to persist as living organisms to survive if excreted into the environment," says Kong.This self-destruct feature can be fine-tuned so that the bacteria fully colonize host cells, provoking a strong response from both humoral and cell-mediated arms of the immune system. Inside host tissues, recombinant Salmonella are able to synthesize protective antigens, releasing their contents when they become unstable and lyse into the intracellular fluid or cytosol.The group demonstrated the effectiveness of this delayed-lysis bacteria in vaccine experiments with a variety of pathogens, including influenza and mycobacteria (causative agent of tuberculosis) and an RASV vaccine developed in the Curtiss lab against infant pneumonia is currently in FDA Phase I clinical trials. This earlier work focused on producing protective protein antigens in a bacterium, which would subsequently release a bolus of these antigens when the bacterial cell lysed within host cells and tissues.In the latest research, the group sought to turn a delayed-lysis Salmonella strain into a universal DNA vaccine delivery vehicle. DNA vaccines stimulate cellular and humoral immune responses to protein antigens through the direct introduction of genetic material, prompting host cells to manufacture specific gene products. This is a crucial advance as it allows for the production of antigens that undergo host cell modification through the addition carbohydrates -- a process known as glycosylation. Such modified antigens, which occur in a broad range of pathogenic viruses, fungi and parasites require synthesis by host cells, rather than by the attenuated bacteria."Here, we were able to deliver a vaccine whose DNA sequence induces the immunized individual to make the protective glycoprotein the way you would during a viral infection," Curtiss says. Previous efforts to achieve this advance for delivery of DNA vacines by bacteria date to 1995, but only now has such work come to fruition.A number of key modifications to the delayed-lysis RASV were required for this feat, and the Kong and Curtiss team has worked intensively over the past 5 years to achieve them. A hyperinvasive form of Salmonella was constructed through recombinant DNA methods in order to maximize the vaccine vector's ability to invade host cells and become internalized.Following host cell uptake, Salmonella are encased in a membrane-bound endosome known as the Salmonella Containing Vacuole. The RASV was further modified to permit escape from the endosome so that the mature bacterium could spew its immunogenic contents into the host cell's cytosol.Finally, further revisions to the Salmonella strain were applied to diminish the pathogen's ability to cause host cell death, which would prevent the DNA vaccine from migrating to the host cell nucleus to induce the synthesis of protective antigens necessary for the immune response.The authors note that their orally-administered RASV is markedly superior to earlier efforts which introduced DNA vaccines by means of intramuscular injection or gene gun. These methods fail to deliver the vaccine to both mucosal tissues and certain internal lymphoid tissues, vital to a sustained, protective immunity. "We can protect mice to doses of influenza that would be lethal were they not effectively immunized," Curtiss says, adding that "RASV safety has been established in mice just two hours old as well as in pregnant and immunodeficient mice."Influenza spreads around the world in seasonal epidemics, resulting in about three to five million yearly cases of severe illness and about 250,000 to 500,000 yearly deaths, rising to millions in some pandemic years. Current manufacture of influenza vaccines requires use of chick embryos or cell culture methods. Global capacity is limited, making sufficient vaccine to immunize everyone impossible. Adding to concerns about managing future naturally occurring influenza epidemics is the potential for bioterrorists to produce weaponized influenza strains created using plasmid-based reverse genetics systems. "Increasing the speed of producing a matching vaccine is key in the context of response to an influenza epidemic," Kong says.The ability to rapidly engineer and scale up effective vaccines for influenza and other potentially lethal pathogens will require innovative approaches to vaccine design, manufacture and application. The universal DNA vaccine platform outlined in the new study represents an important advance."The vast majority of viruses including influenza, measles, mumps and HIV all have glycosylated proteins. You could never deliver protective immunity using a bacterium to produce those protein antigens," Curtiss says. "But now we have the opportunity to produce vaccines against such pathogens," Kong says. Further, the technique permits large quantities of DNA vaccine to be produced rapidly at low cost, freeze-dried and stockpiled to be used when needed.Dr Roy Curtiss is also a professor in the College of Liberal Arts and Sciences, School of Life Sciences. | Genetically Modified | 2,012 |
November 5, 2012 | https://www.sciencedaily.com/releases/2012/11/121105114616.htm | Genetically engineered tomatoes decrease plaque build-up in mice | For the first time, genetically engineered tomato plants produced a peptide that mimics the actions of good cholesterol when eaten, researchers reported at the American Heart Association's Scientific Sessions 2012. | In the study, mice that ate the freeze-dried, ground tomatoes had less inflammation and reduced atherosclerosis (plaque build-up in the arteries)."We have found a new and practical way to make a peptide that acts like the main protein in good cholesterol, but is many times more effective and can be delivered by eating the plant," said Alan M. Fogelman, M.D., senior author of the study and executive chair of the Department of Medicine and director of the Atherosclerosis Research Unit in the David Geffen School of Medicine at UCLA.Researchers genetically engineered the tomatoes to produce 6F, a small peptide that mimics the action of ApoA-1, the chief protein in high density lipoprotein (HDL or "good" cholesterol). They fed the tomatoes to mice that lack the ability to remove low density lipoprotein (LDL or "bad" cholesterol) from their blood and readily develop inflammation and atherosclerosis when consuming a high-fat diet.After the mice ate the tomatoes as 2.2 percent of their Western-style high-fat, calorie-packed diet, those given the peptide-enhanced tomatoes had significantly:"To our knowledge this is the first example of a drug with these properties that has been produced in an edible plant and is biologically active when fed without any isolation or purification of the drug," Fogelman said.Co-authors are Arnab Chattopadhyay, Ph.D.; Mohamad Navab, Ph.D.; Greg Hough, B.S.; David Meriwether, B.S.; Gao Feng, Ph.D.; Victor Grijalva, B.S.; James R. Springstead, Ph.D.; Mayakonda N. Palgunachari, Ph.D.; Ryan Namiri-Kalantari, B.S.; G.M. Anantharamaya, Ph.D.; Robin Farias-Eisner, M.D., Ph.D.; and Srinivasa T. Reddy, Ph.D. Author disclosures are on the abstract.The National Heart, Lung, and Blood Institute funded the study. | Genetically Modified | 2,012 |
October 25, 2012 | https://www.sciencedaily.com/releases/2012/10/121025145233.htm | Isolation of Puerto Rico's manatees affects survival odds | New evidence shows there is no cross-breeding between endangered manatees in Puerto Rico and those in Florida, resulting in less genetic diversity in Puerto Rico's small manatee population and impacting its odds of survival. | The findings, which come from a study of West Indian manatees by the U.S. Geological Survey and Puerto Rico Manatee Conservation Center, could help resource managers make decisions about how to conserve the endangered marine mammal."Wildlife management has been one of the fields to benefit greatly from the ability to determine relatedness of individuals from DNA analysis, allowing management decisions to be based on concrete scientific evidence for genetic diversity and prospects for it to increase," said USGS Director Marcia McNutt. "These results for Puerto Rico's manatees are a wake-up call."One key management concern is the ability of Puerto Rico's manatees to absorb and rebound from population declines. Current estimates suggest as few as 250 individual manatees may currently live in Puerto Rico. Furthermore, the population's genetic diversity is low, a fact which decreases a wildlife population's capacity to adapt to changing conditions and rebound after critical events that can cause deaths, such as hurricanes, boat strikes, or disease.This latest finding -- that Puerto Rico's manatees are genetically isolated -- shows the population's vulnerability to future ups and downs is not being offset by migration from Florida manatees, as was once hoped."Puerto Rico's Antillean manatees have low overall numbers and low genetic diversity, both of which present risks for the population's long-term survival," said Margaret Hunter, Ph.D., a USGS geneticist and lead author of the study. "The lack of gene flow is another risk factor. We detected no signs that the Puerto Rico population is being supplemented by Florida manatees, through migration or breeding. This means that Puerto Rico's population must absorb shocks -- such as environmental change or disease -- on their own. It's a trifecta of genetic vulnerability."In their most recent 5-year review, released in 2007, the U.S. Fish and Wildlife Service recommended that West Indian manatees be downlisted from endangered to threatened, although no decision was made at that time.As of the last status review, it was difficult to determine whether the two populations were mixing. Puerto Rico's manatees were already considered a different subspecies -- the 'Antillean' subspecies, while those in the continental U.S. are the 'Florida' subspecies. Although the distinction had been based on different physical traits observed in the two types of manatees, this study confirms that there is indeed a strong genetic basis to those differences.The research offers a clearer picture of breeding relationships because the research team compared Florida and Puerto Rico using nuclear DNA, which provides enough granular detail about diversity to draw conclusions about current breeding rates. Earlier genetic data on West Indian manatees came from analysis of mitochondrial DNA, a type of genetic material typically used to understand a species' ancient migratory past.Among other findings in the study is the existence of two manatee populations within Puerto Rico itself that do not frequently interbreed. The two genetically different groups provide diversity that may improve the long-term prospects for manatees in Puerto Rico."This study provides solid data that allows us to better understand what Puerto Rico's manatee population faces internally to survive…both as individuals and as a population. It also directs us in developing and implementing future studies in health assessments and habitat use that will enhance current conservation efforts in the island on behalf of the species," said co-author Antonio Mignucci, Ph.D., director of the Puerto Rico Manatee Conservation Center and research professor at Inter American University of Puerto Rico.Puerto Rico's manatees are not only isolated from Florida's population, but have little chance of receiving migrants from other nearby islands. The USGS has been working with the PRMCC and other biologists in Caribbean nations to gather new data about causes of death, habitat use, and breeding among manatees found on the surrounding islands. At this point, Jamaica and the Dominican Republic are believed to have small manatee populations while Guadeloupe, Haiti and the Virgin Islands have no known manatees."The more that we continue to learn about this unique mammal, the better we can enable managers to make decisions that ensure adequate protection," said Bob Bonde, Ph.D., a USGS research biologist and co-author of the research.The study, "Puerto Rico and Florida manatees represent genetically distinct groups," is available online in the journal | Genetically Modified | 2,012 |
October 18, 2012 | https://www.sciencedaily.com/releases/2012/10/121018134001.htm | No antibodies, no problem: Researchers identify how mosquito immune system attacks specific infections | Researchers at the Johns Hopkins Bloomberg School of Public Health have determined a new mechanism by which the mosquitoes' immune system can respond with specificity to infections with various pathogens, including the parasite that causes malaria in humans, using one single gene. Unlike humans and other animals, insects do not make antibodies to target specific infections. According to the Johns Hopkins researchers, mosquitoes use a mechanism known as alternative splicing to arrange different combinations of binding domains, encoded by the same AgDscam gene, into protein repertoires that are specific for different invading pathogens. | The researchers' findings were published October 18 in the journal Mosquitoes and other insects use their primitive innate immune systems to successfully fight infections with a broad spectrum of viruses, bacteria, fungi and parasites, despite the lack of antibodies that are part of the more sophisticated human immune system. The effectiveness of the human immune system is to a large degree based on the ability to produce an enormous variety of antibodies containing different immunoglobulin domains that can specifically tag and label a pathogen for destruction. This great variety of pathogen-binding antibodies is achieved by combining different immunoglobulin gene segments and further mutate them through mechanisms called somatic recombination and hypermutation. While mosquitoes also have genes encoding immunoglobulin domains, they lack these specific mechanisms to achieve pathogen recognition diversity.The Johns Hopkins researchers discovered a different way by which mosquitoes can combine immunoglobulin domains of a single gene called AgDscam (Anopheles gambiae Down Syndrome Cell Adhesion Molecule) to produce a variety of pathogen-binding proteins. The AgDscam gene is subjected to a mechanism called alternative splicing that combines different immunoglobulin domains into mature AgDscam proteins, depending on which pathogen has infected the mosquito. The researchers showed that this alternative splicing is guided by the immune signal transducing pathways (analogous to electrical circuits) that they previously demonstrated to activate defenses against different malaria parasites and other pathogens. While alternative splicing of the AgDscam gene does not nearly achieve the degree of pathogen recognition diversity of human antibodies, it does nevertheless vastly increase the variety of pathogen binding molecules."Using antibodies to fight infection is like fishing with a harpoon -- it's very targeted. The mosquito's innate immune system is more like fishing with a net -- it catches a bit of everything," explained George Dimopoulos, PhD, senior investigator of the study and professor with the Johns Hopkins Malaria Research Institute. "However, we discovered that immune pathway-guided alternative splicing of the AgDscam gene renders the mosquito's immune net, so to speak, more specific than previously suspected. The mosquito's immune system can come up with approximately 32,000 AgDscam protein combinations to target infections with greater specificity."Dimopoulos and his group are developing a malaria control strategy based on mosquitoes that have been genetically modified to possess an enhanced immune defense against the malaria parasite Plasmodium. One obstacle to this approach is the great variety of Plasmodium strains that may interact somewhat differently with the mosquito's immune system."Some of these strains may not be detected by the engineered immune system proteins that mediate their killing. Our new discovery may provide the means to create genetically modified mosquitoes that can target a broader variety of parasite strains, like casting a net rather than shooting with a harpoon," said Dimopoulos.Malaria kills more than 800,000 people worldwide each year. Many are children.The research was supported by grants from the National Institutes of Health/National Institute of Allergy and Infectious Disease, the Calvin A. and Helen H. Lang Fellowship, and the Johns Hopkins Malaria Research Institute. | Genetically Modified | 2,012 |
October 15, 2012 | https://www.sciencedaily.com/releases/2012/10/121015112840.htm | Protein could be key for drugs that promote bone growth | Georgia Health Sciences University researchers have developed a mouse that errs on the side of making bone rather than fat, which could eventually lead to better drugs to treat inflammatory diseases such as rheumatoid arthritis. | Drugs commonly used to treat those types of conditions -- called glucocorticoids -- work by turning down the body's anti-inflammatory response, but simultaneously turn on other pathways that lead to bone loss. The result can lead to osteoporosis and an accumulation of marrow fat, says Dr. Xingming Shi, bone biologist at the GHSU Institute of Molecular Medicine and Genetics.The key to the body developing bone instead of fat, a small protein called GILZ, was shown in cell cultures in 2008. Now, with work by GHSU Graduate Student Guodong Pan, the work has been replicated in an animal model. Pan received the American Society for Bone and Mineral Research's Young Investigator Award for his work at the society's annual meeting Oct. 12-15 in Minneapolis.Bone and marrow fat come from the same biological precursor -- mesynchymal stem cells. "The pathways for bone and fat have a reciprocal relationship, so we needed to find the key that disrupts the fat production pathway, which would then instead encourage bone growth," Shi says.GILZ, Shi and Pan say, was already a known mediator of the anti-inflammatory response of glucocorticoids, and the protein also mediates bone production. Shi's early research had shown that glucocorticoids enhance bone formation in the lab because of a short "burst" of GILZ.The protein works by inhibiting the way cells regulate fat production and turn on fat-producing genes, Shi says. "When you permanently express GILZ, the fat pathway is suppressed, so the body chooses to produce bone instead.""We found that when we overexpressed the protein in these mice, it increased bone formation," Pan added. "This supports our original hypothesis that GILZ mediates the body's response to glucocorticoids and encourages bone growth." In fact, the genetically modified mice showed a significant increase in bone mineral density and bone volume as well, he found."That means GILZ is a potential new anti-inflammatory drug candidate that could spare people from the harmful effects associated with glucocorticoid therapy," Pan saidLong-term goals, Shi said, are developing the GILZ-like pill that is anti-inflammatory and protects or even increases bone production. | Genetically Modified | 2,012 |
October 11, 2012 | https://www.sciencedaily.com/releases/2012/10/121011085336.htm | DNA confirms genetically distinct lion population for Ethiopia | A team of international researchers has provided the first comprehensive DNA evidence that the Addis Ababa lion in Ethiopia is genetically unique and is urging immediate conservation action to preserve this vulnerable lion population. | While it has long been noted that some lions in Ethiopia have a large, dark mane, extending from the head, neck and chest to the belly, as well as being smaller and more compact than other lions, it was not known until now if these lions represent a genetically distinct population.The team of researchers, led by the University of York, UK, and the Max Planck Institute for Evolutionary Anthropology, Germany, has shown that captive lions at the Addis Ababa Zoo in Ethiopia are, in fact, genetically distinct from all lion populations for which comparative data exists, both in Africa and Asia.The researchers compared DNA samples from 15 Addis Ababa Zoo lions (eight males and seven females) to lion breeds in the wild. The results of the study, which also involved researchers from Leipzig Zoo and the Universities of Durham and Oxford, UK, are published in the Principal Investigator Professor Michi Hofreiter, of the Department of Biology at the University of York, said: "To our knowledge, the males at Addis Ababa Zoo are the last existing lions to possess this distinctive mane. Both microsatellite and mitochondrial DNA data suggest the zoo lions are genetically distinct from all existing lion populations for which comparative data exist."We therefore believe the Addis Ababa lions should be treated as a distinct conservation management unit and are urging immediate conservation actions, including a captive breeding programme, to preserve this unique lion population."The lion (One of the regions with a declining lion population is Ethiopia. In addition to a few hundred wild lions scattered throughout the country, 20 lions are kept in the Addis Ababa Zoo. These lions belonged to the collection of the late emperor of Ethiopia, Haile Selassie. He established the zoo in 1948 and the seven founder lions (five males and two females) are claimed to have been captured in south-western Ethiopia, although their geographical origin is controversial.In their study, the team of researchers recommend establishing a captive breeding programme as a first step towards conserving this unique lion population.Lead author Susann Bruche, now with Imperial College London, but who conducted the research with the Max Planck Institute for Evolutionary Anthropology, said: "A great amount of genetic diversity in lions has most likely already been lost, largely due to human influences. Every effort should be made to preserve as much of the lion's genetic heritage as possible. We hope field surveys will identify wild relatives of the unique Addis Ababa Zoo lions in the future, but conserving the captive population is a crucial first step. Our results show that these zoo lions harbour sufficient genetic diversity to warrant a captive breeding programme."It has previously been suggested that no lions comparable to those at Addis Ababa Zoo still exist in the wild, mainly due to hunting for their mane. However, the researchers say that according to the Ethiopian authorities, lions with a similar appearance to those at Addis Ababa Zoo still exist in the east and north-east of the country, notably in the Babille Elephant Sanctuary near Harar and southwards to Hararghe. These regions, the researchers say, should be prioritised for field surveys.Professor Hofreiter said: "A key question is which wild population did the zoo lions originate from and whether this wild population still exists; this would obviously make it a priority for conservation. What is clear is that these lions did not originate in the zoo, but come from somewhere in the wild -- but not from any of the populations for which comparative data is available." | Genetically Modified | 2,012 |
October 5, 2012 | https://www.sciencedaily.com/releases/2012/10/121005123815.htm | Genotyping helps identify source of clinic infection outbreak | Researchers from East Carolina University used a new technique of genotyping to identify the source of a hematology clinic outbreak of | Using repetitive sequence-based polymerase chain reaction ( Diversilab® system), the first time this genotyping method was used in an The use of new technology to match the genetic material in the bacteria established the source of the outbreak; however, since The outbreak involved four young sickle cell patients. Since all four patients had long-term lines implanted (i.e., ports used to deliver medication into the bloodstream), they were probably exposed to While reviewing the infection control practices of the unit, preparation of intravenous medications by one nurse, who was involved in the care of all four patients, was found to be the only breach in safe practices. During the period of infection, this healthcare worker prepared injections at the sink counter. It's likely that the fluid bag being used to prepare injections became contaminated when the worker washed her hands.As a result of the investigation, all of the water aerators were removed from the faucets and educational information stressing that sinks were not to be used as work spaces were distributed to staff. Since the changes, no new cases of "This study demonstrates the efficacy of using genotyping technology in identifying the source of the outbreak," said Muhammad Salman Ashraf, MD, assistant professor at The Brody School of Medicine at East Carolina University. "But it also points to the need for proper infection control practice in clinic settings, and that faucet aerators should be avoided in all healthcare facilities, especially those caring for immunosuppressed patients." | Genetically Modified | 2,012 |
October 2, 2012 | https://www.sciencedaily.com/releases/2012/10/121002092839.htm | 'Superweeds' linked to rising herbicide use in GM crops, study finds | A study published this week by Washington State University research professor Charles Benbrook finds that the use of herbicides in the production of three genetically modified herbicide-tolerant crops -- cotton, soybeans and corn -- has actually increased. | This counterintuitive finding is based on an exhaustive analysis of publicly available data from the U.S. Department of Agriculture's National Agriculture Statistics Service. Benbrook's analysis is the first peer-reviewed, published estimate of the impacts of genetically engineered (GE) herbicide-resistant (HT) crops on pesticide use.In the study, which appeared in the open-access, peer-reviewed journal "Resistant weeds have become a major problem for many farmers reliant on GE crops, and they are now driving up the volume of herbicide needed each year by about 25 percent," Benbrook said.The annual increase in the herbicides required to deal with tougher-to-control weeds on cropland planted to GE cultivars has grown from 1.5 million pounds in 1999 to about 90 million pounds in 2011.Herbicide-tolerant crops worked extremely well in the first few years of use, Benbrook's analysis shows, but over-reliance may have led to shifts in weed communities and the spread of resistant weeds that force farmers to increase herbicide application rates (especially glyphosate), spray more often and add new herbicides that work through an alternate mode of action into their spray programs. | Genetically Modified | 2,012 |
September 27, 2012 | https://www.sciencedaily.com/releases/2012/09/120927141306.htm | 'Semi-dwarf' trees may enable a green revolution for some forest crops | The same "green revolution" concepts that have revolutionized crop agriculture and helped to feed billions of people around the world may now offer similar potential in forestry, scientists say, with benefits for wood, biomass production, drought stress and even greenhouse gas mitigation. | Researchers at Oregon State University recently outlined the latest findings on reduced height growth in trees through genetic modification, and concluded that several advantageous growth traits could be achieved for short-rotation forestry, bioenergy, or more efficient water use in a drier, future climate.This approach runs contrary to conventional wisdom and centuries of tree breeding, which tried to produce forest trees that grow larger and taller, the researchers note. But just as the green revolution in agriculture helped crops such as wheat and rice produce more food on smaller, sturdier plants, the opportunities in forestry could be significant."Research now makes it clear that genetic modification of height growth is achievable," said Steven Strauss, an OSU professor of forest genetics. "We understand the genes and hormones that control growth not only in crop plants, but also in trees. They are largely the same."In a study published in The range and variation in genetic modification can be accurately observed and selected for, based on hormone and gene expression levels, to allow production of trees of almost any height.For example, for ornamental purposes it would be possible to grow a miniature poplar, or even a Douglas-fir, as a potted plant.And because height growth, in competition for sunlight, is a primary mechanism that trees use to compete for survival, there would be reduced concern about use of such genetically modified trees in a natural environment. On a long-term basis they would be unable to compete, shaded by larger trees and ultimately they would die out.Scientists could also produce trees that might have a larger root mass, which should make them more drought-resistant, increase water use efficiency, increase elimination of soil toxins and better sequester carbon. This could be useful for greenhouse gas mitigation, bioremediation or erosion control.Smaller trees could also be selected that have sturdier trunks for some uses in short-rotation plantation forestry, significantly reducing the number of trees blown down by wind. And shorter, thicker and straighter trunks might create higher-value wood products in many tree species, Strauss said.Some semi-dwarf trees produced by conventional tree breeding techniques are already an important part of the horticulture industry, allowing easier harvesting of fruit and higher yields. Genetic modification could add new characteristics and more scientific precision to the process, researchers said."The main limitation is the onerous regulatory structure for genetically-modified plants in the United States," Strauss said. "Even short, safe and beneficial trees are unlikely to be able to bear the high costs and red tape inherent to obtaining regulatory approval."This research has been supported by the U.S. Department of Energy, U.S. Department of Agriculture, National Science Foundation, and industry members of the Tree Biosafety and Genomics Research Cooperative at OSU. | Genetically Modified | 2,012 |
September 26, 2012 | https://www.sciencedaily.com/releases/2012/09/120926152931.htm | Molecular process in fat cells that influences stress and longevity identified | As part of their ongoing research investigating the biology of aging, the greatest risk factor for type 2 diabetes and other serious diseases, scientists at Joslin Diabetes Center have identified a new factor -- microRNA processing in fat tissue -- which plays a major role in aging and stress resistance. This finding may lead to the development of treatments that increase stress resistance and longevity and improve metabolism. | The findings appear in the Sept. 5 online edition of Over the past several years, it has become clear that fat cells (adipocytes) are more than just repositories to store fat. Indeed, fat cells secrete a number of substances that actively influence metabolism and systemic inflammation. Previous studies have found that reducing fat mass by caloric restriction (CR) or surgical or genetic means can promote longevity and stress resistance in species from yeast to primates. However, little is known about how CR and fat reduction produce these beneficial effects. This study investigated one type of molecular mediator -- change in microRNAs (miRNAs) and the processing enzymes required to make them- that is influenced by aging and reversed by caloric restriction. miRNAs are involved in the formation of mature RNA.Based on studies conducted using human cells, mice and Caloric restriction, which has been shown to prolong lifespan and improve stress resistance in both mice and worms, prevents this decline of Dicer, and in the case of the mice, restore miRNAs to levels observed in young mice. Conversely, exposure of adipocytes to major stressors associated with aging and metabolic diseases, including toxic agents, Dicer levels decreased. Mice and worms engineered to have decreased Dicer expression in fat showed increased sensitivity to stress, a sign of premature aging. By contrast, worms engineered to "overexpress" Dicer in the intestine (the adipose tissue equivalent in worms) had greater stress resistance and lived longer.Overall, these studies showed that regulation of miRNA processing in adipose-related tissues plays an important role in longevity and an organism's ability to respond to age-related and environmental stress. "This study points to a completely new mechanism by which fat might affect lifespan and is the first time that anyone has looked at fat and miRNAs as factors in longevity," according to co-author T. Keith Blackwell, MD, PhD, co-head of Joslin's Section on Islet Cell and Regenerative Biology and Professor of Pathology at Harvard Medical School.Based on this study, Blackwell suggests that "finding ways to improve miRNA processing to keep miRNA levels up during aging might have a role in protecting against the stresses of everyday life and the development of age- and stress-related disease."Dr. Kahn and the study investigators are currently working on ways to genetically control Dicer levels in the fat tissues of mice, to create mouse models that are more or less resistant to stress. "We would love to find drugs that would mimic this genetic manipulation to produce a beneficial effect," says Dr. Kahn. "If we can better understand the biology of aging, we might also understand how age impacts diabetes," says Kahn.Study co-authors include Marcelo A. Mori, Prashant Raghavan, Jeremie Boucher, Stacey Robida-Stubbs, Yazmin Macotela, Steven J. Russell, and T. Keith Blackwell of Joslin; and James L. Kirkland and Thomas Thomou of the Mayo Clinic. | Genetically Modified | 2,012 |
September 5, 2012 | https://www.sciencedaily.com/releases/2012/09/120905135346.htm | Study in mice discovers injection of heat-generating cells reduces belly fat | The injection of a tiny capsule containing heat-generating cells into the abdomens of mice led those animals to burn abdominal fat and initially lose about 20 percent of belly fat after 80 days of treatment. | Researchers conducting the study were surprised to see that the injected cells even acted like "missionaries," converting existing belly fat cells into so-called thermogenic cells, which use fat to generate heat.Over time, the mice gained back some weight. But they resisted any dramatic weight gain on a high-fat diet and burned away more than a fifth of the cells that make up their visceral fat, which surrounds the organs and is linked to higher risk for Type 2 diabetes, cancer and heart disease.The scientists took advantage of the heat-generating properties of a so-called good fat in the body, brown fat, to cut back on the white fat cells that compose the visceral fat that tends to accumulate in the belly.The scientists combined those brown fat thermogenic cells with genetically modified cells missing an enzyme that leads to visceral fat growth. The engineered cells were placed inside a gel-like capsule that allowed for release of its contents without triggering an immune response."With a very small number of cells, the effect of the injection of this capsule was more pronounced at the beginning, when the mice dramatically lost about 10 percent of their weight. They gained some weight back after that. But then we started to look at how much visceral fat was present, and we saw about a 20 percent reduction in those lipids. Importantly, other nontreated peripheral or subcutaneous fat, which has some beneficial health effects, remained the same. That's what we want," said Ouliana Ziouzenkova, assistant professor of human nutrition at Ohio State University and lead author of the study."We observed the mice for 80 days after injection and the capsule didn't break or cause any scarring or inflammation. This suggests it's a clean, safe potential therapy for obesity," added Ziouzenkova, also an investigator in Ohio State's Comprehensive Cancer Center and the Center for Clinical and Translational Science. Studies in larger animals would be needed before trials in humans could begin, she said.If this were someday approved for humans, Ziouzenkova said such a therapy would be best suited to patients who develop visceral fat with aging, aren't able to exercise and shouldn't dramatically reduce their calories because that can cause the loss of beneficial subcutaneous fat. She also noted that anti-obesity drugs for humans currently on the market can reduce body weight by about 10 to 15 percent, but also have side effects.The research is published in a recent issue of the journal A year ago, Ziouzenkova's lab identified an enzyme in mice that relates to fat accumulation after consumption of a high-fat diet, and she recently published a paper indicating that mice lacking that enzyme could stay lean even while eating excess fat. She applied those findings in this work by using the genetically modified cells that are missing that enzyme to potentially help boost the ability of brown fat cells to burn up visceral fat.For this study, she collaborated with Ohio State chemists to create the capsules. They are composed of alginate-poly-L-lysine, a compound that creates enough of a barrier to encapsulate cells without signaling the immune system that it should react to a foreign object in the body, while also enabling nutrient supply to the encapsulated cells for their long-term survival.The researchers used three groups of normal mice for the study, feeding them all a high-fat diet for 90 days. After that, five mice received no treatment, five were treated with empty capsules and five received an injection of active capsules containing genetically engineered cells. The capsules were injected into two areas of visceral fat in their abdomens.The mice continued to eat a high-fat diet for another 80 days. The mice receiving no treatment continued to gain weight in those 80 days, while the mice receiving thermogenic cells lost weight for 23 days and then began to gain it back, eventually maintaining a steady weight even after continuing to eat excessive saturated fat. Mice receiving empty capsules also lost some weight, but the researchers determined in a separate pilot study that the sham injections did not reduce visceral fat.The researchers examined visceral fat pads from the mice and determined that overall, lipid content was at least 20 percent lower in mice treated with active capsules compared to the placebo injection group of mice.A closer look at exactly what was going on in the animals' cells showed that the injected cells produced high levels of a protein called Ucp1, which burns fat, suggesting that this protein assisted in the visceral fat reduction.By tagging the injected cells with a fluorescent protein, the scientists could use imaging technology to track the cells in the body; this not only benefited the research, but also provides a way to safely remove these capsules if needed, Ziouzenkova noted."The injected cells were perfectly inversely correlated with lipids -- so the more injected cells we have capable of burning fat, the more fat gets burned," she said. "These injected cells worked almost like missionaries, starting to convert host cells and turning them into thermogenic cells."Because that creation of heat could be uncomfortable inside a human body, the researchers analyzed the treated mice further to see if the thermogenesis in the belly would produce effects similar to hot flashes."Heat production was higher in injected animals, but it was not dramatically higher. So there is some kind of response, but it seems not to be at a magnitude impairing a patient's well-being," Ziouzenkova said. "The animals were also moving less than noninjected animals, but in spite of that, they were still able to lose visceral fat. Their glucose tolerance improved, as well, which is probably related to reduced visceral fat."Ziouzenkova said she hopes to design additional capsules to target a variety of diseases beyond obesity.This work was supported by the American Heart Association Great Rivers Affiliate, the National Institutes of Health, a pilot industry partnership grant at the Center for Clinical and Translational Science (funded by the National Center for Research Resources), the Ohio State College of Education and Human Ecology (EHE), a Food Innovation Center Seed grant and an EHE dissertation fellowship.Ziouzenkova collaborated with several Ohio State scientists on this research, including L. James Lee, director of the NSF Nanoscale Science and Engineering Center for Affordable Nanoengineering of Polymeric Biomedical Devices (NSEC); and Sanjay Rajagopalan, Chandan Sen and Sashwati Roy of the Davis Heart and Lung Research Institute (DHLRI). Additional co-authors include Fangping Yang and David DiSilvestro of the Department of Human Nutrition; Xulang Zhang of the NSEC; Andrei Maiseyeu of the DHLRI; Georgeta Mihai, Santosh Maurya and Muthu Periasamy of the Department of Physiology & Cell Biology; and Rumana Yasmeen and Valerie Bergdall of University Laboratory Animal Resources, all at Ohio State; and Gregg Duester of the Sanford-Burnham Medical Research Institute in La Jolla, Calif. | Genetically Modified | 2,012 |
August 30, 2012 | https://www.sciencedaily.com/releases/2012/08/120830065737.htm | Bacterium transforms into weapon against sleeping sickness | Scientists of the Antwerp Institute of Tropical Medicine (ITG) opened a new front against the cause of sleeping sickness. This parasite is transmitted between humans by tsetse flies. The researchers learned a bacterium living in those flies how to produce antibodies against the parasite. Application in the field is still a long way of, but the technique shows quite some promise. | Sleeping sickness is caused by trypanosomes, parasites being transmitted by the bite of a tsetse fly.The World Health Organization estimates the yearly death toll at between 10,000 and 20,000 people. On top of that, the parasite also infects cattle, causing considerable economic loss. Many small African farmers depend on their cattle.Without treatment, an infection is irrevocably fatal. Unfortunately, many poor people present at the hospital only in a late stadium. At that time the Trypanosoma parasites have lodged themselves in the brain, behind the notorious blood-brain barrier that keeps most drugs out. Arsenic compounds can pass the barrier and kill the parasite, but they also kill five per cent of the patients. New drugs are not in the pipeline.Besides the parasite, one may also attack its vector, the tsetse fly. But insecticides may be detrimental to the environment, certainly in the long run. Therefore scientists look for alternative strategies. For instance genetically modified insects that are incapable of being infected by the parasite, or do not transmit it. But germline transformation of tsetse flies is unfeasible. To do so, one must be able to handle the eggs, but tsetse flies do not lay eggs, they directly bring forth a larva.Therefore, the Antwerp researchers took another road. Tsetse flies harbour, as is the case with many insects, resident bacteria. One of them, Sodalis glossinidius (literally: companion of the tsetse fly) exclusively lives in tsetse flies. And it can be cultivated in the lab. De Vooght was the first to genetically modify the bacterium so it produces, and excretes, a very efficient type of antibody, called a nanobody. She identified two different secretory pathways that transported the nanobodies out of the bacterium. She also demonstrated that the bacterium was not hampered by its modification, so it can stand its ground amidst non-modified, 'wild type' congeners inside the fly.Next, with antibiotics she cleared tsetse flies of their wild type bacteria and replaced those by the modified bacteria. These successfully colonized the flies and started producing nanobodies. The nanobodies also were present in the midgut, where the sleeping sickness parasite also is to be found.De Vooght demonstrated the feasibility of the technique, but it still needs some development before it can be used to control sleeping sickness in the field. For instance, the antibodies now produced by the bacteria, are directed against a form of the parasite occurring in humans, not in flies. This is simply because this antibody was available, while the one against the fly form still has to be developed. De Vooght: "We wanted to demonstrate first that the technique works in principle. Now we have achieved that, we can tackle the technical details."To the scientists it is just as important that symbiotic bacteria producing all kinds of substances are a means to getting insight into the interactions between disease-causing organisms and their insect vectors. The Antwerp researchers already demonstrated that the sleeping sickness parasite interferes with the saliva production of tsetse flies, forcing them to bite more humans than they otherwise would do. Insight in that kind of interactions might be instrumental to opening new ways of attacking diseases. | Genetically Modified | 2,012 |
August 31, 2012 | https://www.sciencedaily.com/releases/2012/08/120831083315.htm | No more sneezing: Allergen-free house plants | New research published in BioMed Central's open access journal BMC Plant Biology shows how targeting two bacterial genes into an ornamental plant ( | In a collaborative project, researchers from the Instituto de Biología Molecular y Celular de Plantas (IBMCP) and BIOMIVA S.L. (Spain) modified The modified DNA was injected into Dr Luis Cañas, one of the researchers from IBMCP explained, "The ipt enzyme catalyzes the rate-limiting step for cytokinin biosynthesis in plants and consequently extra ipt, provided transgenically, produces more cytokinin and prevents the plant cells from aging. In addition, the use of an anther-specific promoter from pea driving the expression of a bacterial gene (ribonuclease), prevents the development of male progenitor cells into anthers and pollen, resulting in pollen-free flowers."The generation of long-life plants is good news for the gardener who wants a display of flowers for as long as possible and the lack of pollen not only is great for hay fever sufferers but also prevents accidental release of the transgenes into the environment. However the extra cytokinin does not protect against owners forgetting to water their plants... | Genetically Modified | 2,012 |
August 26, 2012 | https://www.sciencedaily.com/releases/2012/08/120826170404.htm | Simplifying genetic codes to look back in time | Tokyo Institute of Technology researchers show simpler versions of the universal genetic code can still function in protein synthesis. In addition to understanding early primordial organisms, the research could lead to applications preventing non-natural genetically modified materials from entering the natural world. | Daisuke Kiga and co-workers at the Department of Computational Intelligence and Systems Science at Tokyo Institute of Technology, together with researchers across Japan, have shown that simpler versions of the universal genetic code, created by knocking out certain amino acids, can still function efficiently and accurately in protein synthesis [1].The researchers conducted experiments altering the genetic code in a test tube. They removed the amino acid tryptophan and discovered that the resulting simplified code could still generate proteins as before.By knocking out individual amino acids and observing the effects, scientists will be able to understand how early primordial organisms may have functioned and evolved. There will be also numerous applications for simplified genetic strains in laboratory experiments, which could potentially prevent non-natural genetically modified materials from entering the natural world.Daisuke Kiga and co-workers of the Department of Computational Intelligence and Systems Science at Tokyo Institute of Technology, together with researchers across Japan, have shown that simpler versions of the universal genetic code -- created by knocking out certain amino acids -- can still function efficiently and accurately in protein synthesis. The researchers conducted cell-free experiments altering the genetic code.All current life forms on Earth have 20 amino acids in their genetic code. However, scientists believe that this was not always the case, and that organisms evolved from simpler genetic codes with fewer amino acids. Amino acids are linked in accordance with codons -- a 3-letter combination of the four base nucleotides (G, A, T and C) in a genetic code. There are 64 possible codons, and so most amino acids are produced by several different codons, except for tryptophan and methionine, which are generated by just one codon each. Tryptophan is thought to be the most recent amino acid to become part of the universal genetic code.Kiga and his team took the codon for tryptophan, and reassigned it to code for the amino acid alanine instead. They discovered the resulting simplified code could still generate proteins as before. The researchers also reassigned another codon originally for the amino acid cysteine and replaced it with serine. This simplified code without cysteine was able to synthesize an active enzyme.By knocking out individual amino acids and observing the effects, scientists will be able to understand how early primordial organisms may have functioned and evolved. There are also numerous applications for simplified genetic codes in laboratory experiments and clinical trials.Before emergence of the current universal genetic code, primitive organisms that may have used only 19 amino acids could benefit from horizontal gene transfer, where cells transfer genetic material between one another. This is a key method used by bacteria to develop resistance to drugs. An organism with the current universal genetic code for 20 amino acids would have competitive advantages in its ability to synthesize proteins, but could not engage in genetic transfer with the rest of the population. Only when a suitably large gene pool of organisms with 20 amino acids is available could horizontal transfer occur between these life forms and they could then thrive. This implies that organisms with a simpler genetic code could be used as a barrier in laboratory experiments, preventing new genetically modified strains from escaping to the natural world.[1] A. Kawahara-Kobayashi et al. Simplification of the genetic code: restricted diversity of genetically encoded amino acids. Nucleic Acids Research (2012) As yet unpublished. | Genetically Modified | 2,012 |
August 20, 2012 | https://www.sciencedaily.com/releases/2012/08/120820121044.htm | Genetically engineered algae for biofuel pose potential risks | Algae are high on the genetic engineering agenda as a potential source for biofuel, and they should be subjected to independent studies of any environmental risks that could be linked to cultivating algae for this purpose, two prominent researchers say. | Writing in the August 2012 issue of the journal A critical baseline concern is whether genetically engineered algae would be able to survive in the wild, said Allison Snow, professor of evolution, ecology and organismal biology at Ohio State University and lead author of the paper."If they're grown in big, open ponds, which is mainly what were talking about, could the newer types of microalgae get out into nature and mingle? We need to know if they can survive and whether they can hybridize or evolve to become more prolific when they get out of a controlled environment," Snow said."If they can survive, we also need to know whether some types of genetically engineered blue-green algae, for example, could produce toxins or harmful algal blooms -- or both," Snow noted.And because algae are so small and could be dispersed by rough weather or wildlife activity, biologists worry that any transgenes they contain to enhance their growth and strength could be transferred to other species in a way that could upset a fragile ecosystem."The applications are new and the organisms are less well-known. They range from being very tame 'lab rats' that won't survive in nature to wild organisms that can presumably cross with each other unless some measures are taken to prevent crossing. It's a very new situation," Snow said.Snow co-authored the article with aquatic ecologist Val Smith, a professor in the Department of Ecology and Evolutionary Biology at the University of Kansas.Snow has a history in this area of research. She led a study in 2002 that was the first to show that a gene artificially inserted into crop plants to fend off pests could migrate to weeds in a natural environment and make the weeds stronger. She also has served on national panels that monitor and make recommendations about the release of genetically engineered species into the environment.There are a lot of unknowns about this area of research and development in microalgae, and that's largely because algae don't have the breeding history that, say, corn and soybeans have, Snow said. In addition, few details are publicly available because much of this information remains confidential as businesses compete to be the first to commercialize their genetically altered algae."We're hoping to reach several audiences -- including ecologists, molecular biologists and biotech business owners -- and bring them together. There's a community of people like me who study genetically engineered crops and how they interact with the environment, and we need to get this started with algae."There's a lot of hype and speculation about algae as a biofuel source, and it's hard to gauge exactly what's going on. We see many indications, especially funding, that private companies and the government have decided this is important and worth pursuing," Snow said. "So much will depend on the economics of it. Whether you can get a lot of energy out of algae depends on these breakthroughs with biology, technology, or both."In the same way that certain crop plants are bred with genes to help them repel pests and tolerate harsh conditions, different species of algae are likely being genetically engineered to grow rapidly because mass quantities of these tiny species will be needed to produce adequate fuel supplies.The authors recommend, for starters, a comparative examination of genetically engineered algae strains intended for large-scale cultivation with their natural counterparts to determine the basic differences between the two. They also acknowledged that genetically engineered algae might be equipped with so-called "suicide genes" that would make it impossible for the algae to survive a release into the wild."If such precautions are taken in lieu of thorough environmental assessments, more information should be required to ensure their long-term success and to prevent (genetically engineered) algae from evolving to silence or overcome biological traits that are designed to kill them," the authors wrote.Snow also noted that before genetically engineered crop plants can be commercialized, they are grown in various outdoor environments to test their endurance under different conditions. The permitting process for these plots helps inform the government and the public about these agricultural efforts. Even if the exact genes used to engineer these crops are protected as proprietary information, the species and new traits they carry are made public."With algae, this can all happen in a greenhouse because they're so small. That means they're not really accessible for scientists to find out what companies are working with, and it's going to be like that until very late in the process," Snow said.And to be clear, Snow said she and Smith are not looking to hinder these efforts."We're trying to be constructive and get the word out, to get the conversation going," she said. | Genetically Modified | 2,012 |
August 16, 2012 | https://www.sciencedaily.com/releases/2012/08/120816201616.htm | Organisms cope with environmental uncertainty by guessing the future | In uncertain environments, organisms not only react to signals, but also use molecular processes to make guesses about the future, according to a study by Markus Arnoldini et al. from ETH Zurich and Eawag, the Swiss Federal Institute of Aquatic Science and Technology. The authors report in | Most organisms live in ever-changing environments, and are at times exposed to adverse conditions that are not preceded by any signal. Examples for such conditions include exposure to chemicals or UV light, sudden weather changes or infections by pathogens. Organisms can adapt to withstand the harmful effects of these stresses. Previous experimental work with microorganisms has reported variability in stress responses between genetically identical individuals. The results of the present study suggest that this variation emerges because individual organisms take random decisions, and such variation is beneficial because it helps organisms to reduce the metabolic costs of protection without compromising the overall benefits.The theoretical results of this study can help to understand why genetically identical organisms often express different traits, an observation that is not explained by the conventional notion of nature and nurture. Future experiments will reveal whether the predictions made by the mathematical model are met in natural systems. | Genetically Modified | 2,012 |
August 16, 2012 | https://www.sciencedaily.com/releases/2012/08/120816141527.htm | Clear links found between inflammation, bacterial communities and cancer | What if a key factor ultimately behind a cancer was not a genetic defect but ecological? | Ecologists have long known that when some major change disturbs an environment in some way, ecosystem structure is likely to change dramatically. Further, this shift in interconnected species' diversity, abundances, and relationships can in turn have a transforming effect on health of the whole landscape -- causing a rich woodland or grassland to become permanently degraded, for example -- as the ecosystem becomes unstable and then breaks down the environment.For this reason, it should come as no surprise that a significant disturbance in the human body can profoundly alter the makeup of otherwise stable microbial communities co-existing within it and that changes in the internal ecology known as the human microbiome can result in unexpected and drastic consequences for human health.A report published in the August 16 online edition of the journal The authors of the study were Janelle C. Arthur, Ernesto Perez-Chanona, Marcus Mühlbauer, Sarah Tomkovich, Joshua M. Uronis, Ting-Jia Fan, Christian Jobin, Arlin B. Rogers, Jonathan J. Hansen, and Temitope O. Keku from the University of North Carolina at Chapel Hill; Barry J. Campbell and Jonathan M. Rhodes from the University of Liverpool; Turki Abujamel and Alain Stintzi from the University of Ottawa; Belgin Dogan and Kenneth W. Simpson from Cornell University; and Anthony A. Fodor from the University of North Carolina at Charlotte.In a series of experiments conducted with mice prone to intestinal inflammation, the researchers found that inflammation itself causes significant simplification in diverse communities of gut microbes and allows new bacterial populations to establish major footholds. Among the bacterial taxa invading the disturbed intestinal ecosystem, the research team found a greatly increased presence of The researchers noted that the mouse results may have implications for human health as well, as they also found an Anthony Fodor, an associate professor of bioinformatics at UNC Charlotte, a co-author on this study and a member of NIH's Human Microbiome Project consortium, has also been involved in another study that analyzed bacterial populations in relation to colorectal cancer, recently published in the journal of the International Society for Microbial Ecology (ISME, May 24). This study examined 70 human subjects and found that many taxa, including some pathogens broadly related to Though Fodor believes the finding, by showing a correlation between microbial diversity and cancer in humans, may have potential for future medical diagnoses, he cautions that the results were far too preliminary to be used to draw any solid conclusions."As is usual in human studies, we didn't have cause and effect" Fodor noted. "We don't know if microbes are somehow causing conditions to shift in the gut that would cause cancer or if there are conditions that are associated with cancer that would increase the openness of the gut to particular microbes."In contrast, Fodor said the current Science study "is all about mechanism."" Generally, to get at mechanism, you need to be able to do experiments and you can't do experiments in humans," he said. "The mouse model studies allow us to test theories of causation." Fodor remarked that the Jobin lab's mouse studies were quite elegant in narrowing in on a causal connection between microbes and colorectal cancer. "It's amazing how cleanly this came out."The first step in the study established a clear connection between the physiological condition of intestinal inflammation and a subsequent change in microbial communities in the gut.Key to the studies were IL10-/- mice, a mouse model that is genetically prone to gut inflammation because it is bred to lack a gene that suppresses the inflammatory response. Using a technique that allows researchers to identify bacterial varieties by examining variants in a specific gene (16S rRNA), the team compared bacterial communities in the inflamed guts of IL10-/- mice with those in healthy normal ("wild type") mice. They found that the diversity of different kinds of bacteria was significantly lower in the mice with genetically-facilitated inflammation. Among the IL10-/- mice, however, the team found little difference in microbial diversity between mice that simply had inflammation and those that also had cancer, indicating the inflammation was the critical factor affecting microbe populations."A shift in the microbial community is associated with inflammation," Fodor noted. "It is interesting that the microbial community is actually changing with the disease state, which indicates that it is either responding to or contributing to the disease state."Despite the overall drop in diversity, the team found that the presence of The researchers were curious whether or not they could find evidence for a cause-and-effect relationship between The experiment seemed to show that it was the presence of From reviewing the literature on The team then looked to human subjects to see if there was a specific association of pks-containing bacteria with colorectal cancer. The team examined 24 healthy people, 35 with irritable bowel disease (which includes gut inflammation) and 21 with colorectal cancer."Remarkably, we found the bug with pks in only 5 out of 24 controls (20% in healthy people), but if you look at people with inflammatory bowel disease, the bug and pks were present in 14 out of 35 (40%,) and with people with colorectal cancer it was 15 out of 21 (66.7%)," Fodor noted."These are exciting results because they suggest there may be a direct link between changes in the gut microbiome and the progression from inflammation to cancer," said Fodor. "If we can understand the pathways by which pathogens damage host cells within the context of host inflammation, we may be able to formulate a personalized approach to cancer prevention in which particular pathogenic taxa or genes are targeted in vulnerable human sub-populations." | Genetically Modified | 2,012 |
August 13, 2012 | https://www.sciencedaily.com/releases/2012/08/120813115530.htm | Scientists use light to 'tag and track' genetic processes | In a new study, UT Dallas researchers outline how they used fluorescent molecules to "tag" DNA and monitor a process called DNA looping, a natural biological mechanism involved in rearranging genetic material in some types of cells. | The UT Dallas "tag and track" method not only sheds light on how DNA loops form, but also might be adapted to screen drugs for effectiveness against certain viruses that shuffle genetic material, such as HIV.Until now, scientists primarily had "snapshots" of the initial and final stages of DNA loop formation, with only limited information about what happens during the intermediate steps, said Dr. Stephen Levene, professor of bioengineering, molecular and cell biology, and phyiscs at UT Dallas. He is senior author of the study, published online and in an upcoming issue of the journal "Scientists have known for more than 30 years that DNA looping is an important part of molecular biology and gene regulation, but until our work, there have been few serious attempts to understand the basic biophysics of the process," Levene said.DNA looping is a mechanism common in many instances of natural gene-splicing. Proteins within cells -- or proteins made by invading viruses -- latch onto specific docking points on a DNA molecule. They bring those points together to form a loop, and then snip out the genetic material between the points while reconnecting the now-loose ends.DNA loop formation is especially important in organisms whose genetic material is circular, including some bacteria and viruses. Human DNA is linear, but the possibility that DNA looping takes place in human cells is an ongoing area of investigation, Levene said.Levene and UT Dallas doctoral student Massa Shoura, the lead author of the paper, used a protein called Cre in their experiments. Cre is made by a virus that infects bacteria and is so good at forming DNA loops and excising genetic material that scientists routinely use it to delete genes from laboratory animals, which are then used to study the role of genes in human disease.Levene and Shoura engineered isolated segments of DNA to contain Cre's docking points. They also inserted into those points a molecule that fluoresces when exposed to certain wavelengths of light. By monitoring the changes in fluorescence, the researchers could watch the steps of the loop formation.The information the researchers have gleaned is not only useful for understanding basic biology and genetics, but also might lead to more efficient methods for screening potential new drugs for anti-HIV activity.Once inside a host cell, HIV produces an enzyme similar to Cre, called an integrase. As its name suggests, the integrase slices into the host's DNA and inserts HIV's genetic material."Our fluorescent-tag technique could be used in the lab to more closely examine how HIV inserts itself into the host's genome," Shoura said. "By labeling and monitoring the process, we also could test drugs designed to interfere with the integrase.""We estimate that using fluorescence-based methods such as this for drug screening could be as much as 10,000 times more efficient than methods that are currently used," Levene said.Other UT Dallas researchers from the Department of Molecular and Cell Biology who participated in the study were senior scientist Dr. Alexandre Vetcher; doctoral students Stefan Giovan, Farah Bardai and Anusha Bharadwaj; and former undergraduate student Matthew Kesinger. The National Institutes of Health and the National Science Foundation funded the research. | Genetically Modified | 2,012 |
August 9, 2012 | https://www.sciencedaily.com/releases/2012/08/120809190725.htm | Copper facilitates prion disease, scientists show | Many of us are familiar with prion disease from its most startling and unusual incarnations -- the outbreaks of "mad cow" disease (bovine spongiform encephalopathy) that created a crisis in the global beef industry. Or the strange story of Kuru, a fatal illness affecting a tribe in Papua New Guinea known for its cannibalism. Both are forms of prion disease, caused by the abnormal folding of a protein and resulting in progressive neurodegeneration and death. | While exactly how the protein malfunctions has been shrouded in mystery, scientists at The Scripps Research Institute now report in the journal "This conclusively shows that copper plays a role in the misfolding of the protein, but is not essential to that misfolding," said Scripps Research Professor Michael Oldstone, who led the new study."We've known for many years that prion proteins bind copper," said Scripps Research graduate student Owen Siggs, first author of the paper with former Oldstone lab member Justin Cruite. "But what scientists couldn't agree on was whether this was a good thing or a bad thing during prion disease. By creating a mutation in mice that lowers the amount of circulating copper by 60 percent, we've shown that reducing copper can delay the onset of prion disease."Unlike most infections, which are caused by bacteria, viruses, or parasites, prion disease stems from the dysfunction of a naturally occurring protein."We all contain a normal prion protein, and when that's converted to an abnormal prion protein, you get a chronic nervous system disease," said Oldstone. "That occurs genetically (spontaneously in some people) or is acquired by passage of infectious prions. Passage can occur by eating infected meat; in the past, by cannibalism in the Fore population in New Guinea through the ingestion or smearing of infectious brains; or by introduction of infectious prions on surgical instruments or with medical products made from infected individuals."When introduced into the body, the abnormal prion protein causes the misfolding of other, normal prion proteins, which then aggregate into plaques in the brain and nervous system, causing tremors, agitation, and failure of motor function, and leads invariably to death.The role of copper in prion disease had previously been studied using chelating drugs, which strip the metals from the body -- an imprecise technique. The new study, however, turned to animal models engineered in the lab of Nobel laureate Bruce Beutler while at The Scripps Research Institute. (Beutler is currently director of the Center for the Genetics of Host Defense at UT Southwestern.)The Beutler lab had found mice with mutations disrupting copper-transporting enzyme ATP7A. The most copper-deficient mice died "Copper is something we can't live without," said Siggs. "Like iron, zinc, and other metals, our bodies can't produce copper, so we absorb small amounts of it from our diet. Too little copper prevents these enzymes from working, but too much copper can also be toxic, so our body needs to maintain a fine balance. Genetic mutations like the one we describe here can disrupt this balance."In the new study, both mutant and normal mice were infected with Rocky Mountain Laboratory mouse scrapie, which causes a spongiform encephalopathy similar to mad cow disease. The control mice developed illness in about 160 days, while the mutant mice, lacking the copper-carrying gene, developed the disease later at 180 days.Researchers also found less abnormal prion protein in the brains of mutant mice than in control mice, indicating that copper contributed to the conversion of the normal prion protein to the abnormal disease form. However, all the mice eventually died from disease.Oldstone and Siggs note the study does not advocate for copper depletion as a therapy, at least not on its own. However, the work does pave the way for learning more about copper function in the body and the biochemical workings of prion disease.In addition to Siggs, Cruite, Beutler, and Oldstone, authors of the paper "Disruption of copper homeostasis due to a mutation of Atp7a delays the onset of prion disease," are Xin Du formerly of Scripps Research and currently of the University of California, San Diego (UCSD); Sophie Rutschmann, formerly of Scripps Research and currently of Imperial College London; and Eliezer Masliah of UCSD.This work was supported by the National Institutes of Health (award numbers HHSN272200700038C, AG04342, AG18440, AG022074, and NS057096) and by the General Sir John Monash Foundation. | Genetically Modified | 2,012 |
August 8, 2012 | https://www.sciencedaily.com/releases/2012/08/120808142001.htm | Chronic exposure to staph bacteria may be risk factor for lupus | Chronic exposure to even small amounts of staph bacteria could be a risk factor for the chronic inflammatory disease lupus, Mayo Clinic research shows. Staph, short for | The findings are published online this month in "We think this protein could be an important clue to what may cause or exacerbate lupus in certain genetically predisposed patients," Dr. Chowdhary says. "Our hope is to confirm these findings in lupus patients and hopefully prevent flares."Another key question is whether treating at-risk people to eradicate staph can prevent lupus from forming in the first place. Lupus occurs when the immune system attacks tissues and joints. It may affect virtually any part of the body and can be tough to diagnose because it often mimics other ailments. There is no cure, only treatment to control symptoms. Lupus is more commonly diagnosed in women, African-Americans, Hispanics, Asians and people 15 to 40.The cause is often unknown; it appears people genetically predisposed to lupus may develop it when something in the environment triggers it, such as infections, certain drugs or even sunlight.Physicians do not really know what causes lupus, so the discovery of the staph protein's possible role is exciting, Dr. Chowdhary says.In the mice studied, a staph protein known as a staphylococcal enterotoxin B, or SEB, activated autoreactive T and B lymphocytes, a type of white blood cells, leading to an inflammatory illness mirroring lupus. Research on people has shown that carrying staph bacteria is linked to autoimmune diseases such as psoriasis, Kawasaki disease and graulomatosis with polyangiitis.The lupus study was funded by the National Institutes of Health, an American College of Rheumatology Research and Education Foundation Career Development Bridge Funding Award, a Ronald F. Kinney Executive Dean for Research Career Development Award from Mayo Foundation and a Mayo Clinic Research Early Career Development Award.The research team included Ashenafi Tilahun; Chad Clark; Joseph Grande, M.D., Ph.D.; and Govindarajan Rajagopalan, Ph.D., all of Mayo Clinic. | Genetically Modified | 2,012 |
August 2, 2012 | https://www.sciencedaily.com/releases/2012/08/120802122512.htm | Upgrading synthetic biology's toolkit: New method could enable reprogramming of mammalian cells | Through the assembly of genetic components into "circuits" that perform logical operations in living cells, synthetic biologists aim to artificially empower cells to solve critical problems in medicine, energy and the environment. To succeed, however, they'll need far more reliable genetic components than the small number of "off-the-shelf" bacterial parts now available. | Now a new method developed by Assistant Professor Ahmad S. Khalil (BME), Professor James J. Collins (BME, MSE, SE) and collaborators at Harvard Medical School, Massachusetts General Hospital and MIT could significantly increase the number of genetic components in synthetic biologists' toolkit and, as a result, the size and complexity of the genetic circuits they can build. The development could dramatically enhance their efforts not only to understand how biological organisms behave and develop, but also to reprogram them for a variety of practical applications.Described in the August 2 online edition of With funding from the Howard Hughes Medical Institute, the Defense Advanced Research Projects Agency and other sources, the research team built their synthetic genetic circuit parts from a class of proteins, known as zinc fingers, which can be programmed to bind desired DNA sequences. The modularity of the new parts enables a wide range of functions to be engineered, the construction of much larger and more complex genetic circuits than what's now possible with bacteria-based parts, and ultimately, the development of much more powerful applications."Our research may lead to therapeutic applications, such as the dynamic modification and control of genes and genetic networks that are important in human disease," said Khalil. Potential medical applications include stem cell therapeutics for a wide variety of injuries and diseases and in-cell devices and circuits for diagnosing early stages of cancer and other diseases. The new method may also equip groups of cells to perform higher-order computational tasks for processing signals in the environment in sensing applications." | Genetically Modified | 2,012 |
July 18, 2012 | https://www.sciencedaily.com/releases/2012/07/120718090713.htm | Discovery of 'hopping' of bacterial enzyme gives insight into gene expression | UC Santa Barbara researchers' discovery of a variation of an enzyme's ability to "hop" as it moves along DNA, modifying the genetic material of a bacteria -- and its physical capability and behavior -- holds much promise for biomedical and other scientific applications. | The "We're trying to figure out what is it in the cell that's driving those changes," said Adam Pollak, first author of the paper.The formation of these pili is driven by an epigenetic mechanism -- a "tagging" done by the enzyme DNA adenine methyltransferase (Dam), which acts on a specific sequence of DNA, called GATC sites (Guanine-Adenine-Thymine-Cytosine). The tagging signals the formation of these -- appendages a mechanism similar to that in humans, where tagging directs the formation of tissues for different organs from the same DNA. This tagging is part of a broader field, called epigenetics, where modifications made to the genome are heritable and regulate the expression of genes.Where the prevailing belief used to be that the enzyme Dam slid down only one side of the bacteria's double-helixed DNA looking for these GATC sites, according to the researchers, Dam can actually "hop" to one or more such sites on both sides of the double helix."It moves along, finds a site, and methylates that; but it turns around, reorients itself, and methylates the other side," said Norbert Reich, UCSB professor of chemistry and biochemistry.Using several strands of genetically engineered DNA of various lengths and differing distances between the sites of methylation, the researchers found that the hopping of Dam may occur more often, depending on the clustering of sites; e.g., it is more likely to occur when two sites are within 10 to 200 base pairs of each other. Clustered GATC sites are strongly associated with gene regulation, while an isolated GATC site on the double helix is associated with the copying of DNA. According to the authors' findings, the longer the enzyme goes without locating the GATC sequence of molecules, the less likely that it will undergo this new variation of hopping, but the introduction of a GATC sequence will stimulate the mechanism once again.According to the paper, hopping can explain the efficiency by which DNA-modifying enzymes can find their recognition sites, despite the presence of an overwhelming amount of non-specific DNA; as well as how enzymes can modify more than one site, despite opposing strand orientations.The research capitalizes on decades of observation of "If we had inhibitors that could prevent the switching, we wouldn't have urinary tract infections, for instance," said Pollak.The same research group recently reported a similar mechanism in humans, which is disrupted in certain forms of leukemia. | Genetically Modified | 2,012 |
July 16, 2012 | https://www.sciencedaily.com/releases/2012/07/120716151648.htm | Genetically engineered bacteria prevent mosquitoes from transmitting malaria | Researchers at the Johns Hopkins Malaria Research Institute have genetically modified a bacterium commonly found in the mosquito's midgut and found that the parasite that causes malaria in people does not survive in mosquitoes carrying the modified bacterium. The bacterium, | "In the past, we worked to genetically modify the mosquito to resist malaria, but genetic modification of bacteria is a simpler approach," said Marcelo Jacobs-Lorena, PhD, senior author of the study and a professor with Johns Hopkins Bloomberg School of Public Health. "The ultimate goal is to completely prevent the mosquito from spreading the malaria parasite to people."With the study, Jacobs-Lorena and his colleagues found that the engineered "We demonstrate the use of an engineered symbiotic bacterium to interfere with the development of Malaria kills more than 800,000 people worldwide each year. Many are children.The authors of "Fighting malaria with engineered symbiotic bacteria from vector mosquitoes" are Sibao Wang, Anil K. Ghosh, Nicholas Bongio, Kevin A. Stebbings, David J. Lampe and Marcelo Jacobs-Lorena.The research was supported by National Institute of Allergy and Infectious Diseases, the Bill & Melinda Gates Foundation, the Johns Hopkins Malaria Research Institute and the Bloomberg Family Foundation. | Genetically Modified | 2,012 |
July 16, 2012 | https://www.sciencedaily.com/releases/2012/07/120716142731.htm | Low-cal diet's effects seen in fly brain, mouthpart | A novel technique for measuring tiny, rapid-fire secretions in the brains and mouthparts of fruit flies (drosophila) is providing insights into the beneficial effects of eating less -- information that ultimately could help people suffering from neuromuscular disorders. | Using the method, researchers uncovered never-before-seen brain chemistry that helps explain why fruit flies genetically manipulated to mimic conditions such as Parkinson's disease and myasthenia gravis are more vigorous and live longer when fed a restricted diet.Published in June by Senior author Benjamin Eaton, Ph.D., assistant professor of physiology, says the results demonstrate how limiting calories may be therapeutic for people with various syndromes.Lead author Joel Rawson, Ph.D., and the Eaton team developed a novel system to analyze the impact of diet on life span and motor behavior as well as on neurotransmission, which is believed to underlie most neurological disorders in humans.Flies on the low-calorie diet showed a 100 percent increase in the release of brain chemicals, which are called neurotransmitters, from their neurons. These chemicals carry signals from one nerve cell to another across gaps called synapses. The brain has millions of synapses that are believed to be the critical structures required for normal brain function. Diseases such as Parkinson's harm them irreparably.Furthermore the chemicals were secreted at critical locations. "Diet restriction increased the neurotransmitters released at synapses called neuromuscular junctions," Dr. Eaton said. "These synapses, which form on muscle, transmit nerve impulses from the brain to muscles, resulting in movement. If neuromuscular junctions degenerate, resulting in the release of less neurotransmitter, then muscle activity diminishes. This is observed in diseases such as myasthenia gravis and amyotrophic lateral sclerosis (ALS)."The observation that diet could directly affect the amount of neurotransmitter secreted by the neuron was a novel observation that had not been seen previously."People have seen that diet has effects on the nervous system, but the nuts and bolts of what it is doing to neurons have not been established," Dr. Eaton said. ""We believe we have shown a novel and important effect."The team genetically engineered a single pair of motor neurons to develop neurodegenerative disease, resulting in a decrease of the flies' ability to extend the proboscis, which they use to gather food. The team then dissected the head to locate the appropriate muscles on the proboscis and quantified the neurotransmitter activity occurring there, which continues to take place even after death."We went into the very muscles that that these motor neurons controlled and analyzed neurotransmission using electrodes," Dr. Eaton said. "We showed diet can rescue proboscis extension by increasing the amount of neurotransmitter released. This suggests that diet could be an important therapy for improving muscle function during motor diseases such as ALS."Next up is to define the proteins in neurons that are being altered by diet restriction, he said. | Genetically Modified | 2,012 |
July 5, 2012 | https://www.sciencedaily.com/releases/2012/07/120705172041.htm | How a protein meal tells your brain you're full | Feeling full involves more than just the uncomfortable sensation that your waistband is getting tight. Investigators reporting online on July 5th in the Cell Press journal | Food intake can be modulated through mu-opioid receptors (MORs, which also bind morphine) on nerves found in the walls of the portal vein, the major blood vessel that drains blood from the gut. Specifically, stimulating the receptors enhances food intake, while blocking them suppresses intake. Investigators have now found that peptides, the products of digested dietary proteins, block MORs, curbing appetite. The peptides send signals to the brain that are then transmitted back to the gut to stimulate the intestine to release glucose, suppressing the desire to eat.Mice that were genetically engineered to lack MORs did not carry out this release of glucose, nor did they show signs of 'feeling full', after eating high-protein foods. Giving them MOR stimulators or inhibitors did not affect their food intake, unlike normal mice.Because MORs are also present in the neurons lining the walls of the portal vein in humans, the mechanisms uncovered here may also take place in people."These findings explain the satiety effect of dietary protein, which is a long-known but unexplained phenomenon," says senior author Dr. Gilles Mithieux of the Université de Lyon, in France. "They provide a novel understanding of the control of food intake and of hunger sensations, which may offer novel approaches to treat obesity in the future," he adds. | Genetically Modified | 2,012 |
June 28, 2012 | https://www.sciencedaily.com/releases/2012/06/120628193020.htm | Programmable DNA scissors found for bacterial immune system | Genetic engineers and genomics researchers should welcome the news from the Lawrence Berkeley National Laboratory (Berkeley Lab) where an international team of scientists has discovered a new and possibly more effective means of editing genomes. This discovery holds potentially big implications for advanced biofuels and therapeutic drugs, as genetically modified microorganisms, such as bacteria and fungi, are expected to play a key role in the green chemistry production of these and other valuable chemical products. | Jennifer Doudna, a biochemist with Berkeley Lab's Physical Biosciences Division and professor at the University of California (UC) Berkeley, helped lead the team that identified a double-RNA structure responsible for directing a bacterial protein to cleave foreign DNA at specific nucleotide sequences. Furthermore, the research team found that it is possible to program the protein with a single RNA to enable cleavage of essentially any DNA sequence."We've discovered the mechanism behind the RNA-guided cleavage of double-stranded DNA that is central to the bacterial acquired immunity system," says Doudna, who holds appointments with UC Berkeley's Department of Molecular and Cell Biology and Department of Chemistry, and is an investigator with the Howard Hughes Medical Institute (HHMI). "Our results could provide genetic engineers with a new and promising alternative to artificial enzymes for gene targeting and genome editing in bacteria and other cell types."Doudna is one of two corresponding authors of a paper in the journal Bacterial and archaeon microbes face a never-ending onslaught from viruses and invading circles of nucleic acid known as plasmids. To survive, the microbes deploy an adaptive-type nucleic acid-based immune system that revolves around a genetic element known as CRISPR, which stands for Clustered Regularly Interspaced Short Palindromic Repeats. Through the combination of CRISPRs and associated endonucleases, called CRISPR-associated -- "Cas" -- proteins, bacteria and archaeons are able to utilize small customized crRNA molecules (for CRISPR-derived RNA) to target and destroy the DNA of invading viruses and plasmids.There are three distinct types of CRISPR/Cas immunity systems. Doudna and her colleagues studied the Type II system which relies exclusively upon one family of endonucleases for the targeting and cleaving of foreign DNA, the Cas9 proteins."For the Type II CRISPR/Cas system, we found that crRNA connects via base-pairs with a trans-activating RNA (tracrRNA), to form a two-RNA structure," Doudna says. "These dual RNA molecules (tracrRNA:crRNA) direct Cas9 proteins to introduce double-stranded DNA breaks at specific sites targeted by the crRNA-guide sequence."Doudna and her colleagues demonstrated that the dual tracrRNA:crRNA molecules can be engineered as a single RNA chimera for site-specific DNA cleavage, opening the door to RNA-programmable genome editing."Cas9 binds to the tracrRNA:crRNA complex which in turn directs it to a specific DNA sequence through base-pairing between the crRNA and the target DNA," Doudna says. "Microbes use this elegant mechanism to cleave and destroy viruses and plasmids, but for genome editing, the system could be used to introduce targeted DNA changes into the genome.Doudna notes that the "beauty of CRISPR loci" is that they can be moved around on plasmids."It is well-established that CRISPR systems can be transplanted into heterologous bacterial strains," she says. "Also, there is evidence to suggest that CRISPR loci are horizontally transferred in nature."Doudna and her colleagues are now in the process of gathering more details on how the RNA-guided cleavage reaction works and testing whether the system will work in eukaryotic organisms including fungi, worms, plants and human cells."Although we've not yet demonstrated genome editing, given the mechanism we describe it is now a very real possibility," Doudna says.This work was funded primarily by the Howard Hughes Medical Institute, the Austrian Science Fund and the Swedish Research Council. | Genetically Modified | 2,012 |
June 20, 2012 | https://www.sciencedaily.com/releases/2012/06/120620133359.htm | Trouble on the horizon for genetically modified crops? | Pests are adapting to genetically modified crops in unexpected ways, researchers have discovered. The findings underscore the importance of closely monitoring and countering pest resistance to biotech crops. | Resistance of cotton bollworm to insect-killing cotton plants involves more diverse genetic changes than expected, an international research team reports in the journal To decrease sprays of broad-spectrum insecticides, which can harm animals other than the target pests, cotton and corn have been genetically engineered to produce toxins derived from the bacterium Bt toxins kill certain insect pests but are harmless to most other creatures including people. These environmentally friendly toxins have been used for decades in sprays by organic growers and since 1996 in engineered Bt crops by mainstream farmers.Over time, scientists have learned, initially rare genetic mutations that confer resistance to Bt toxins are becoming more common as a growing number of pest populations adapt to Bt crops.In the first study to compare how pests evolve resistance to Bt crops in the laboratory vs. the field, researchers discovered that while some the of the lab-selected mutations do occur in the wild populations, some mutations that differ markedly from those seen in the lab are important in the field.Caterpillars of the cotton bollworm, Bruce Tabashnik, head of the department of entomology at the University of Arizona College of Agriculture and Life Sciences, who co-authored the study, considers the findings an early warning to farmers, regulatory agencies and the biotech industry."Scientists expected the insects to adapt, but we're just finding out now how they're becoming resistant in the field," Tabashnik said.To avoid surprises, researchers have exposed cotton bollworm populations to Bt toxins in controlled lab experiments and studied the genetic mechanisms by which the insects adapt."We try to stay ahead of the game," he said. "We want to anticipate what genes are involved, so we can proactively develop strategies to sustain the efficacy of Bt crops and reduce reliance on insecticide sprays. The implicit assumption is what we learn from lab-selected resistance will apply in the field."That assumption, according to Tabashnik, had never been tested before for resistance to Bt crops.Now for the first time, the international team gathered genetic evidence from pests in the field, enabling them to directly compare the genes involved in the resistance of wild and lab-reared populations.They found some resistance-conferring mutations in the field were the same as in lab-reared pests, but some others were strikingly different."We found exactly the same mutation in the field that was detected in the lab," Tabashnik said. "But we also found lots of other mutations, most of them in the same gene and one in a completely different gene."A major surprise came when the team identified two unrelated, dominant mutations in the field populations. "Dominant" means that one copy of the genetic variant is enough to confer resistance to Bt toxin. In contrast, resistance mutations characterized before from lab selection are recessive -- meaning it takes two copies of the mutation, one provided by each parent, to make an insect resistant to Bt toxin."Dominant resistance is more difficult to manage and cannot be readily slowed with refuges, which are especially useful when resistance is recessive," Tabashnik said.Refuges consist of plants that do not have a Bt toxin gene and thus allow survival of insects that are susceptible to the toxin. Refuges are planted near Bt crops with the goal of producing enough susceptible insects to dilute the population of resistant insects, by making it unlikely two resistant insects will mate and produce resistant offspring.According to Tabashnik, the refuge strategy worked brilliantly against the pink bollworm in Arizona, where this pest had plagued cotton farmers for a century, but is now scarce.The dominant mutations discovered in China throw a wrench in the refuge strategy because resistant offspring arise from matings between susceptible and resistant insects.He added that the study will enable regulators and growers to better manage emerging resistance to Bt crops."We have been speculating and using indirect methods to try and predict what would happen in the field. Only now that resistance is starting to pop up in many places is it possible to actually examine resistance in the field. I think the techniques from this study will be applied to many other situations around the world, and we'll begin to develop a general understanding of the genetic basis of resistance in the field."The current study is part of a collaboration funded by the Chinese government, involving a dozen scientists at four institutions in China and the U.S. Yidong Wu at Nanjing Agricultural University designed the study and led the Chinese effort. He emphasized the importance of the ongoing collaboration for addressing resistance to Bt crops, which is a major issue in China. He also pointed out that the discovery of dominant resistance will encourage the scientific community to rethink the refuge strategy.Tabashnik said China is the world's top cotton producer, with about 16 billion pounds of cotton per year. India is number two, followed by the U.S., which produces about half as much cotton as China.In 2011, farmers worldwide planted 160 million acres of Bt cotton and Bt corn. The percentage of cotton planted with Bt cotton reached 75 per cent in the U.S. in 2011, but has exceeded 90 per cent since 2004 in northern China, where most of China's cotton is grown.The researchers report that resistance-conferring mutations in cotton bollworm were three times more common in northern China than in areas of northwestern China where less Bt cotton has been grown.Even in northern China, however, growers haven't noticed the emerging resistance yet, Tabashnik said, because only about 2 percent of the cotton bollworms there are resistant."As a grower, if you're killing 98 percent of pests with Bt cotton, you wouldn't notice anything. But this study tells us there is trouble on the horizon." | Genetically Modified | 2,012 |
June 18, 2012 | https://www.sciencedaily.com/releases/2012/06/120618194948.htm | Link between vitamin C and twin seedlings can increase seed production in crops | Biochemists at the University of California, Riverside report a new role for vitamin C in plants: promoting the production of twins and even triplets in plant seeds. | Daniel R. Gallie, a professor of biochemistry, and Zhong Chen, an associate research biochemist in the Department of Biochemistry, found that increasing the level of dehydroascorbate reductase (DHAR), a naturally occurring enzyme that recycles vitamin C in plants and animals, increases the level of the vitamin and results in the production of twin and triplet seedlings in a single seed.The value of the discovery lies in the potential to produce genetically identical seedlings and increase production of high-value crops."The ability to increase fertility can be extremely useful when the inherent rate of fertility is low or the value of the crop is great, such as corn in which the production of multiple embryos would significantly boost its protein content," Gallie said. "The extra seedlings per seed may also enhance per-seed survival chances for some species."Study results appear in the online journal Just as in humans, twins in plants can be either genetically identical or fraternal. Gallie and Chen discovered that the twins and triplets produced in tobacco plants when vitamin C was increased were true twins or triplets as they were genetically identical.In the lab, the researchers went on to show that injecting plant ovaries with vitamin C was sufficient to produce twins or triplets and that the vitamin causes the zygote, the fertilized egg, to divide into two or even three fertilized egg cells before these cells proceed through subsequent stages of development to produce twins or triplets.Although they used tobacco in their research, Gallie predicts vitamin C could generate twins and triplets in other plants as well."Because the early stages of embryo development are so conserved among plant species, we expect that vitamin C will have a similar effect in almost any plant," he said.A question raised by the study is whether vitamin C might have a similar effect in humans. In contrast to most animals, humans cannot make vitamin C and it must, therefore, be obtained regularly from dietary sources."Although the development of plant and animal embryos differ in many respects, the manner in which the genetically identical twins were produced in our study is similar to that for identical human twins in that it is the very first division of the fertilized egg into two separate cells that produces the two separate embryos, resulting in two seedlings in plants or two fetuses in humans," Gallie said. "Despite the differences in the subsequent development of embryos in plants and humans, the critical effect of vitamin C is on this very first cell division."To Gallie's knowledge, no study linking vitamin C to twins in humans has been carried out to date."Humans are mutants in that we lack the last enzyme in the pathway needed to produce vitamin C," he said.Vitamin C is well known to prevent scurvy, a disease affecting collagen synthesis, iron utilization, and immune cell development. It also improves cardiovascular and immune cell function and is used to regenerate vitamin E. The vitamin is present at high levels in some fruits such as citrus and some green leafy vegetables, but present in low levels in those crops most important to humans such as grains.Vitamin C is as essential for plant health as it is for humans. It serves as an important antioxidant, destroying reactive oxygen species that can otherwise damage or even kill cells. In plants, vitamin C is important for photosynthetic function, in controlling water usage, in providing protection against pollutants such as ozone, and promoting growth.A grant from the University of California Agricultural Experiment Station supported the study.Previously, Gallie and Chen, who helped develop technology to increase vitamin C in plants, showed that a boost of the vitamin can help plants defend themselves against the ravages of ozone -- smog's particularly nasty component. They also showed that reducing DHAR increases a plant's responsiveness to drought conditions. | Genetically Modified | 2,012 |
June 14, 2012 | https://www.sciencedaily.com/releases/2012/06/120614094115.htm | Still capable of adapting: Genetic diversity of 'living fossil' coelacanths | The morphology of coelacanths has not fundamentally changed since the Devonian age, that is, for about 400 million years. Nevertheless, these animals known as living fossils are able to genetically adapt to their environment. | This is described by PD Dr. Kathrin Lampert from the RUB's Department of Animal Ecology, Evolution and Biodiversity along with colleagues from Würzburg, Bremen, Kiel and Dar es Salaam (Tanzania) in the journal Previous genetic studies focused mainly on the biological relationships of coelacanths to lungfish and and vertebrates. In order to assess whether the fish are still able to adapt to new environmental conditions, however, you have to know the genetic diversity within the species. For this purpose, the research team examined 71 specimens from various sites on the east coast of Africa. The researchers analysed genetic markers from the nucleus and from the mitochondria, the powerhouses of the cells.The data generally revealed low genetic diversity. As presumed, the evolution of these animals is only progressing slowly. Nevertheless, certain genetic patterns were only found in certain geographic regions. "We assume that the African coelacanth originally came from around the Comoros Islands, home to the largest known population" Lampert explains. Since then, however, two further, now independent populations have established themselves in South Africa and Tanzania. In addition, the animals around the Comoros belong to two genetically distinct groups. "We have thus been able to show that despite their slow evolutionary rate, coelacanths continue to develop and are potentially also able to adapt to new environmental conditions" says the RUB researcher. "The image of the coelacanth as a passive relic of bygone times should therefore be put into perspective."Coelacanths, | Genetically Modified | 2,012 |
June 12, 2012 | https://www.sciencedaily.com/releases/2012/06/120612115949.htm | Mosquitoes bred to be incapable of transmitting malaria | Mosquitoes bred to be unable to infect people with the malaria parasite are an attractive approach to helping curb one of the world's most pressing public health issues, according to UC Irvine scientists. | Anthony James and colleagues from UCI and the Pasteur Institute in Paris have produced a model of the "Our group has made significant advances with the creation of transgenic mosquitoes," said James, a UCI Distinguished Professor of microbiology & molecular genetics and molecular biology & biochemistry. "But this is the first model of a malaria vector with a genetic modification that can potentially exist in wild populations and be transferred through generations without affecting their fitness."More than 40 percent of the world's population lives in areas where there is a risk of contracting malaria. According to the Centers for Disease Control & Prevention, 300 million to 500 million cases of malaria occur each year, and nearly 1 million people die of the disease annually -- largely infants, young children and pregnant women, most of them in Africa.James said one advantage of his group's method is that it can be applied to the dozens of different mosquito types that harbor and transmit the The researchers conceived their approach through mouse studies. Mice infected with the human form of malaria create antibodies that kill the parasite. James' team exploited the molecular components of this mouse immune-system response and engineered genes that could produce the same response in mosquitoes. In their model, antibodies are released in genetically modified mosquitoes that render the parasite harmless to others."We see a complete deletion of the infectious version of the malaria parasite," said James, a member of the National Academy of Sciences. "This blocking process within the insect that carries malaria can help significantly reduce human sickness and death."He and his colleagues have pioneered the creation of genetically altered mosquitoes that limit the transmission of dengue fever, malaria and other vector-borne illnesses.Alison Isaacs, Nijole Jasinskiene and Mikhail Tretiakov of UCI and Isabelle Thiery, Agnes Zettor and Catherine Bourgouin of the Pasteur Institute contributed to the study, which received support from the National Institute of Allergy & Infectious Diseases -- a National Institutes of Health entity -- through grant number R37 AI029746. | Genetically Modified | 2,012 |
June 11, 2012 | https://www.sciencedaily.com/releases/2012/06/120611193342.htm | Sick from your stomach: Bacterial changes may trigger diseases like rheumatoid arthritis | The billions of bugs in our guts have a newfound role: regulating the immune system and related autoimmune diseases such as rheumatoid arthritis, according to researchers at Mayo Clinic and the University of Illinois at Urbana-Champaign. | Larger-than-normal populations of specific gut bacteria may trigger the development of diseases like rheumatoid arthritis and possibly fuel disease progression in people genetically predisposed to this crippling and confounding condition, say the researchers, who are participating in the Mayo Illinois Alliance for Technology Based Healthcare.The study is published in the April 2012 issue of "A lot of people suspected that gut flora played a role in rheumatoid arthritis, but no one had been able to prove it because they couldn't say which came first -- the bacteria or the genes," says senior author Veena Taneja, Ph.D., a Mayo Clinic immunologist. "Using genomic sequencing technologies, we have been able to show the gut microbiome may be used as a biomarker for predisposition."The roughly 10 trillion cells that make up the human body have neighbors: mostly bacteria that often help, training the immune system and aiding in digestion, for example. The bacteria in the intestines, in addition to a relatively small number of other microorganisms (the gut microbiome), outnumber human cells 10-to-1.Researchers found that hormones and changes related to aging may further modulate the gut immune system and exacerbate inflammatory conditions in genetically susceptible individuals.Nearly 1 percent of the world's population has rheumatoid arthritis, a disease in which the immune system attacks tissues, inflaming joints and sometimes leading to deadly complications such as heart disease. Other diseases with suspected gut bacterial ties include type I diabetes and multiple sclerosis.Researchers with the Mayo Illinois Alliance for Technology Based Healthcare say that identifying new biomarkers in intestinal microbial populations and maintaining a balance in gut bacteria could help physicians stop rheumatoid arthritis before it starts."This study is an important advance in our understanding of the immune system disturbances associated with rheumatoid arthritis. While we do not yet know what the causes of this disease are, this study provides important insights into the immune system and its relationship to bacteria of the gut, and how these factors may affect people with genetic susceptibilities to disease," says Eric Matteson, M.D., chairman of rheumatology at Mayo Clinic, who was not a study author.Dr. Taneja and her team genetically engineered mice with the human gene HLA-DRB1*0401, a strong indicator of predisposition to rheumatoid arthritis. A set of control mice were engineered with a different variant of the DRB1 gene, known to promote resistance to rheumatoid arthritis. Researchers used these mice to compare their immune responses to different bacteria and the effect on rheumatoid arthritis."The gut is the largest immune organ in the body," says co-author Bryan White, Ph.D., director of the University of Illinois' Microbiome Program in the Division of Biomedical Sciences and a member of the Institute for Genomic Biology. "Because it's presented with multiple insults daily through the introduction of new bacteria, food sources and foreign antigens, the gut is continually teasing out what's good and bad."The gut has several ways to do this, including the mucosal barrier that prevents organisms -- even commensal or "good" bacteria -- from crossing the lumen of the gut into the human body. However, when commensal bacteria breach this barrier, they can trigger autoimmune responses. The body recognizes them as out of place, and in some way this triggers the body to attack itself, he says.These mice mimic human gender trends in rheumatoid arthritis, in that females were about three times as likely to generate autoimmune responses and contract the disease. Researchers believe these "humanized" mice could shed light on why women and other demographic groups are more vulnerable to autoimmune disorders and help guide development of new future therapies."The next step for us is to show if bugs in the gut can be manipulated to change the course of disease," Dr. Taneja says.The study was funded by the Mayo-Illinois Alliance for Technology Based Healthcare and a grant from the U.S. Department of Defense.Co-authors include Andres Gomez; Carl Yeoman, Ph.D.; and Margret Berg Miller, Ph.D., all of University of Illinois; David Luckey; Eric Marietta, Ph.D.; and Joseph Murray, M.D., all of Mayo Clinic. | Genetically Modified | 2,012 |
June 6, 2012 | https://www.sciencedaily.com/releases/2012/06/120606193853.htm | Fish show autism-like gene expression in water with psychoactive pharmaceuticals | Psychoactive medications in water affect the gene expression profiles of fathead minnows in a way that mimics the gene expression patterns associated with autism spectrum disorder in genetically susceptible humans, according to research published June 6 in the open access journal | The researchers, led by Michael A. Thomas of Idaho State University, exposed the fish to three psychoactive pharmaceuticals -- fluoxetine, a selective serotonin reuptake inhibitor, or SSR1; venlafaxine, a serotonin-norepinephrine reuptake inhibitor, and carbamazepine, used to control seizures -- at concentrations comparable to the highest estimated environmental levels.They found that the only gene expression patterns affected were those associated with idiopathic autism spectrum disorders, caused by genetic susceptibility interacting with unknown environmental triggers. These results suggest that exposure to environmental psychoactive pharmaceuticals may play a role in the development of autism spectrum disorder in genetically predisposed individuals.Lead researcher Michael A. Thomas remarks, "While others have envisioned a causal role for psychotropic drugs in idiopathic autism, we were astonished to find evidence that this might occur at very low dosages, such as those found in aquatic systems." | Genetically Modified | 2,012 |
June 6, 2012 | https://www.sciencedaily.com/releases/2012/06/120606132312.htm | Tracing the brain's connections: Using rabies virus, researcher tracks inputs to dopamine neurons | A genetically-modified version of the rabies virus is helping scientists at Harvard to trace neural pathways in the brain, a research effort that could one day lead to treatments for Parkinson's disease and addiction. | As described in a paper published on June 7 in the journal "You may be familiar with the term connectome," Uchida explained. "The basic idea is we want to understand the brain in terms of connectivity and the various cell types. In this case, we're examining long-range connections; that is, how other parts of the brain connect directly to dopamine neurons.Dopamine neurons are thought to be important for processing reward and regulating motor output."By understanding their inputs, we might be able to better understand how the function of dopamine neurons is regulated, and, in turn, how addiction happens, and how Parkinson's disease and other motor-control disorders are affected by problems with dopamine neurons," Uchida continued. "And because this application provides us with very quantitative data, it's possible that this is a technique that might be useful in attacking the causes of those diseases."Creating that connectivity diagram, however, is anything but easy.While both the VTA and SNc are known to have high concentrations of dopamine neurons, Uchida chose to examine both areas because the cells in the two regions fire differently."We wanted to know what the difference was, generally," Uchida said. "That's why we compared the inputs to both structures. Based on how other neurons are connected there, we can start to explain why these two regions of the brain do different things."The challenge, however, is that dopamine neurons are packed into relatively small regions with several other cell types. To ensure they were only observing dopamine neurons, researchers turned to an organism more typically known for damaging neurons -- the rabies virus.Before they infect genetically-engineered mice with the rabies virus, however, they first inject the animals with a pair of "helper" viruses. The first causes dopamine neurons to produce a receptor protein, meaning the rabies virus can only infect dopamine neurons, while the second restores the virus' ability to "hop" from one neuron to another.The mice are then infected with a version of the rabies virus that has been genetically-modified to produce a fluorescent protein, allowing researchers to track the virus as it binds with dopamine neurons, and then jumps to the cells that link directly to those neurons.The results, as depicted in images of a mouse's brain showing the wealth of connections to dopamine neurons, show that a number of brain regions -- including some previously unknown areas -- are connected to dopamine neurons."We found some new connections, and we found some that we suspected were there, but that were not well understood," Uchida said. "For example, we found that there are connection between the motor cortex and the SNc, which may be related to SNc dopamine neurons' role in motor control."Other connections, though, were more intriguing," he continued. "We found that the subthalmic nucleus preferentially connects to SNc neurons -- that's particularly important because that region is a popular target for deep brain stimulation as a treatment for Parkinson's."Often used as a treatment for Parkinson's and a variety of other disorders, deep brain stimulation involves implanting a device, called a brain pacemaker, into a patient's brain. The device then electrically stimulates specific regions of the brain, helping to mitigate symptoms of the disease."The mechanism for why deep brain stimulation works is not completely understood," Uchida said. "There was speculation that it might have been inhibiting neurons in the subthalmic nucleus, but our findings suggest, because there is a direct connection between those neurons and dopamine neurons in the SNc, that it is actually activating those neurons. I don't think this explains the entire mechanism for why deep brain stimulation works, but this may be part of it.""This work also offers us a roadmap for other areas we might investigate, so now we can target those areas and record from them," Uchida added. "This is a critical step for future investigations." | Genetically Modified | 2,012 |
May 21, 2012 | https://www.sciencedaily.com/releases/2012/05/120521163845.htm | Modern dog breeds genetically disconnected from ancient ancestors | Cross-breeding of dogs over thousands of years has made it extremely difficult to trace the ancient genetic roots of today's pets, according to a new study led by Durham University. | An international team of scientists analyzed data of the genetic make-up of modern-day dogs, alongside an assessment of the global archaeological record of dog remains, and found that modern breeds genetically have little in common with their ancient ancestors.Dogs were the first domesticated animals and the researchers say their findings will ultimately lead to greater understanding of dogs' origins and the development of early human civilization.Although many modern breeds look like those depicted in ancient texts or in Egyptian pyramids, cross-breeding across thousands of years has meant that it is not accurate to label any modern breeds as "ancient," the researchers said.Breeds such as the Akita, Afghan Hound and Chinese Shar-Pei, which have been classed as "ancient," are no closer to the first domestic dogs than other breeds due to the effects of lots of cross-breeding, the study found.Other effects on the genetic diversity of domestic dogs include patterns of human movement and the impact on dog population sizes caused by major events, such as the two World Wars, the researchers added.The findings were published May 21 in the scientific journal In total the researchers analysed genetic data from 1,375 dogs representing 35 breeds. They also looked at data showing genetic samples of wolves, with recent genetic studies suggesting that dogs are exclusively descended from the grey wolf.Lead author Dr Greger Larson, an evolutionary biologist in Durham University's Department of Archaeology, said the study demonstrated that there is still a lot we do not know about the early history of dog domestication including where, when, and how many times it took place.Dr Larson added: "We really love our dogs and they have accompanied us across every continent."Ironically, the ubiquity of dogs combined with their deep history has obscured their origins and made it difficult for us to know how dogs became man's best friend."All dogs have undergone significant amounts of cross-breeding to the point that we have not yet been able to trace all the way back to their very first ancestors."Several breeds, including Basenjis, Salukis and Dingoes, possess a differing genetic signature, which previous studies have claimed to be evidence for their ancient heritage, the research found.However the study said that the unique genetic signatures in these dogs was not present because of a direct heritage with ancient dogs. Instead these animals appeared genetically different because they were geographically isolated and were not part of the 19th Century Victorian-initiated Kennel Clubs that blended lineages to create most of the breeds we keep as pets today.The study also suggested that within the 15,000 year history of dog domestication, keeping dogs as pets only began 2,000 years ago and that until very recently, the vast majority of dogs were used to do specific jobs.Dr Larson said: "Both the appearance and behavior of modern breeds would be deeply strange to our ancestors who lived just a few hundred years ago."And so far, anyway, studying modern breeds hasn't yet allowed us to understand how, where and when dogs and humans first started this wonderful relationship."The researchers added that DNA sequencing technology is faster and cheaper than ever and could soon lead to further insights into the domestication and subsequent evolution of dogs. | Genetically Modified | 2,012 |
May 9, 2012 | https://www.sciencedaily.com/releases/2012/05/120509111453.htm | Antarctic octopus study shows West Antarctic Ice Sheet may have collapsed 200,000 years ago | Scientists at the University have found that genetic information on the Antarctic octopus supports studies indicating that the West Antarctic Ice Sheet could have collapsed during its history, possibly as recently as 200,000 years ago. | Genes from more than 450 Turquet's octopuses, collected from species in the Southern Ocean that surrounds Antarctica, were analysed to shed new light on how animals disperse across the varied ocean landscape. Adult Turquet's octopuses tend to live in one place and only move to escape predators, leading scientists to believe that creatures from areas either side of Antarctica would be genetically different.The team from Liverpool, in collaboration with National University of Ireland Galway, and La Trobe University, Australia, however, found that the octopuses from Ross and Weddell Seas, which are now separated by the West Antarctic Ice Sheet, are genetically almost identical, suggesting that these two regions may have once been connected. Findings may contribute to recent studies demonstrating the potential impact that increasing global temperatures could have on the changing Antarctica environment.Dr Phill Watts, from the University's Institute of Integrative Biology, explains: "We looked at information gathered by the Census of Antarctic Marine Life, which allowed us to examine genetic data on a scale that had not been done before in this area of the world. We expected to find a marked difference between Turguet's octopuses living in different regions of the ocean, particularly between areas that are currently separated by approximately 10,000km of sea. These creatures don't like to travel and so breeding between the populations in the Ross and Weddell Seas would have been highly unusual."We found, however, that they were genetically similar, suggesting that at some point in their past these populations would have been in contact with each other, perhaps at a time when the oceans were connected and not separated by the West Antarctic Ice Sheet. These findings agree with climate models indicating repeated periods in history when the climate was warmer, which would have released water from the ice and increased the sea levels, allowing dispersal of creatures between the Ross and Weddell Seas."Data on octopuses from other parts of Antarctica, not separated by this particular ice sheet, support the theory that the creatures are genetically different. They found that the depth of the ocean and its currents limited the movement of the octopus in certain areas, as would have been expected for those living on either side of the West Antarctic Ice sheet. This added further evidence that at some point in recent history this particular ice sheet might have collapsed.The research is supported by the Natural Environment Research Council (NERC) and the collaborative scheme for systematic research (CoSyst). It is published in the journal Dr Louise Allcock, from the National University of Ireland, Galway, added: "A previous study has shown evidence that the Ross and Weddell Seas could have been connected. We wanted to investigate whether there was any genetic information that could tell us what the past environment could have been like, and this octopus species, with its large populations around the region and limited movements, was an ideal species to use."The fact that we found more similarities than we did differences supports the theory that the West Antarctic Ice Sheet could have collapsed in the past. It also provides further evidence that scientists should continue to raise awareness about the impact of climate change on Antarctica today." | Genetically Modified | 2,012 |
May 8, 2012 | https://www.sciencedaily.com/releases/2012/05/120508220122.htm | Repeat act: Parallel selection tweaks many of the same genes to make big and heavy mice | Organisms are adapted to their environment through their individual characteristics, like body size and body weight. Such complex traits are usually controlled by many genes. As a result, individuals show tremendous variations and can also show subtle gradations. Researchers from the Max Planck Institute for Evolutionary Biology in Plön have now investigated how evolution alters such traits through selection. To do this, they examined the genomes of mouse lines that were selected independently of each other for extreme body size. | They discovered that a number of genomic regions, or loci, have undergone changes in genes that underlie this genetically complex characteristic. They also discovered many new genes that play a role in the regulation of body weight, which can lead to obesity.The Plön-based researchers obtained mouse lines that have been specifically selected for extreme body weight for 25 years. The mice, which have been bred for over 150 generations, belong to seven different strains and now weigh two to four times more than mice of normal weight. The Max Planck scientists were able to identify a total of 67 loci on the genome that had changed in the heavy mice. The different strains have become so similar in these regions as a result of the extreme artificial selection pressure, that the genomes of the heavier but unrelated animals were more similar at these loci than with their closely related sibling mouse strains of those with normal weight. This clearly indicates that these loci are involved in the regulation of body weight.The discovered loci regulate, among other things, energy balance, metabolic processes and growth. The Interestingly, the genome of mouse populations living in the wild on remote islands, shaped by natural selection, have also changed in similar ways to the animals bred in the laboratory. For example, on the Faroe Islands and St Kilda off the coast of Scotland, mice populations have evolved to be among the largest mice in the world. The researchers have found that island mice retained little variation specifically at the same genomic loci that changed in the heavy laboratory-bred animal strains. These telltale signs suggest that artificial selection in the laboratory changes the same loci in the genome as natural selection.Thus, when complex characteristics must adapt to altered environmental conditions, selection affects many responsible genes simultaneously. These then change in parallel and contribute to varying extents to the organism's capacity for adaptation. In this way, the genetic basis of complex traits can be decoded through parallel selection. | Genetically Modified | 2,012 |
May 8, 2012 | https://www.sciencedaily.com/releases/2012/05/120508112703.htm | Challenges in genetically engineered crop regulatory process | A new innovation can completely reshape an industry-- inspiring both optimism and debate. The development of genetically engineered (GE) crops in the 1980's ignited a buzz in the agricultural community with the potential for higher crop yields and better nutritional content, along with the reduction of herbicide and pesticide use. GE crops grew to play a significant role in the U.S., with more than 160 million acres of farmland used to produce GE crops in 2011. However, the development of new GE crops has recently slowed to a trickle due to litigation over field testing and deregulation. University of Minnesota researchers Esther McGinnis, Alan Smith, and Mary Meyer set out to determine the cause of these litigation lulls responsible for slowing GE progress in the U.S. | Three federal agencies are responsible for regulating plant biotechnology in the United States. The Food and Drug Administration (FDA) oversees food and animal feed safety aspects of GE crops. The Environmental Protection Agency (EPA) is responsible for crops engineered to produce pesticidal substances. Lastly, the U.S. Department of Agriculture's Animal and Plant Health Inspection Service (APHIS) regulates the planting of GE crops under the Plant Protection Act, introduced in 2000, to consolidate related responsibilities previously spread across various legislative statutes.APHIS regulates GE crops if the donor organism, recipient organism, or vector or vector agent meets the plant pest definition or the APHIS administrator believes the organism to be a plant pest. The agency's regulatory decisions have met much criticism in the last decade, inspiring the U of M research team to determine if and where APHIS may have gone wrong. The team used past lawsuits as case studies to determine whether APHIS failed to recognize the environmental impacts of GE crops and made legal errors in failing to comply with the sometimes strict procedures of U.S. environmental law.After rising exponentially in the mid-1980s, the first commercially grown GE crop, the Flavr Savr tomato, was approved for sale in the U.S. in 1994. Many farmers since then, adopted GE crops as their own, excited by the prospects of scientific advancement and financial reward.GE crop testing declined rapidly in 2003 in response to the first lawsuit. "Before that time, APHIS was dealing with a pretty heavy case load," says McGinnis. "Their compliance with NEPA may have slipped and left them vulnerable to lawsuits."NEPA, the National Environmental Policy Act, is a U.S. national policy that was established in 1969 to promote environmental protection. NEPA requires environmental agencies to keep an in-depth administrative record of their actions that validates the agency's rationale in reaching regulatory decisions. The lack of transparency in creating these administrative records has been a point of criticism APHIS has faced in recent years.McGinnis and her fellow researchers also pointed out that many of the lawsuits used in their study demonstrate that APHIS failed to differentiate between traditional GE crops, such as corn, soybeans, and cotton, and new GE crops presenting considerable regulatory challenges.Take the genetic engineering of creeping bentgrass, for example. This weedy, wind-pollinated perennial raises unique gene flow concerns that aren't seen in more traditional herbicide-tolerant crops. APHIS has failed to distinguish novel GE crops like this one and hold them to the rigorous evaluation standards required by environmental law, which has led to lawsuits that have grounded the GE crop regulatory process to a halt."APHIS needs to prioritize its resources. It needs to be spending more time regulating novel crops," says McGinnis. "I'm certainly not advocating more regulation of traditional agronomic crops. Really, it's about focusing on these novel crops that raise more issues."APHIS has recently announced plans to streamline their regulatory review process of GE crops, and plans on implementing several efficiency improvements. These include executing more defined deadlines, better resource management, and earlier opportunity for public involvement."If APHIS can solicit public comment earlier in the regulatory process, it can more efficiently incorporate stakeholder concerns into either the environmental assessment or the environmental impact statement that it prepares in conjunction with its regulatory decision," says McGinnis.While APHIS says it has already begun to apply new, more efficient process steps and more defined deadlines, changes to public engagement have yet to be implemented. The agency's complete set of revised procedures go into effect after the plans are published in the Federal Register. | Genetically Modified | 2,012 |
May 7, 2012 | https://www.sciencedaily.com/releases/2012/05/120507154103.htm | Delayed female sexual maturity linked to longer lifespan in mice | An intriguing clue to longevity lurks in the sexual maturation timetable of female mammals, Jackson Laboratory researchers and their collaborators report. | Jackson researchers including Research Scientist Rong Yuan, Ph.D., had previously established that mouse strains with lower circulating levels of the hormone IGF1 at age six months live longer than other strains. In research published May 7 in the "This suggests a genetically regulated tradeoff -- delayed reproduction but longer life -- that is at least partially mediated by IGF1," Yuan says.The researchers conclude that IGF1 may co-regulate female sexual maturation and longevity. They showed that mouse strains derived from wild populations carry specific gene variants that delay sexual maturation, and they identified a candidate gene, Nrip1, involved in regulating sexual maturation that may also affect longevity by controlling IGF1 levels.Yuan notes that researchers in England recently showed that higher levels of IGF1 and other hormones in girls are associated with earlier age of menarche (onset of menstruation). In the newly published research, Yuan and colleagues used the biological benchmark of vaginal patency (VP) as indicator of sexual maturity in female mice.Mice from the inbred strain C57BL/6J, also known as "Black 6," showed 9 percent lower IGF1, 6 percent delayed age of VP and 24 percent extended lifespan compared to a Black 6 substrain that carries a gene variation that increases IGF1.Using a technique called haplotype mapping, the researchers screened genetic and physiological data for 31 different inbred mouse strains and found genes that regulate female sexual maturation and lifespan, on Chromosomes 4 and 16. They showed that wild-derived mouse strains share a genetic profile associated with delayed VP and increased longevity, and identified a candidate gene, Nrip1, that controls IGF1 and age of VP.Yuan is a research scientist in the laboratory of Professor Luanne Peters and a member of the leadership team for the Aging Center at The Jackson Laboratory. | Genetically Modified | 2,012 |
April 29, 2012 | https://www.sciencedaily.com/releases/2012/04/120429234637.htm | Bioluminescent technology for easy tracking of GMO | It is important to be able to monitor genetically modified (GM) crops, not only in the field but also during the food processing chain. New research published in BioMed Central's open access journal | In agriculture GM crops have been bred to improve crop yield or viability. For example some are resistant to herbicides or viruses. They are also used in the pharmaceutical industry to produce proteins such as collagen. However there is a constant debate about the safety of these crops and whether the human-made transgenes might enter the wild population by cross-fertilization.and produce herbicide resistant weeds.Careful handling and sampling techniques are required to assess the GM content of a crop. The most common technique is polymerase chain reaction (PCR), however, this involves complex extraction procedures and rapid thermocycling, both of which require specific equipment. To overcome these problems researchers from Lumora Ltd. assessed whether they could use LAMP to amplify DNA at a constant temperature and use BART to identify GM-specific DNA in real time.Dr Guy Kiddle from Lumora, who led the research, explained that LAMP-BART was able to detect as little as 0.1% GM contamination of maize, and, compared to PCR, was more tolerant of contaminating polysaccharides, meaning that the DNA clean-up process did not need to be as thorough. He commented, "This method requires only basic equipment for DNA extraction, and a constant temperature for DNA amplification and detection. Consequently LAMP-BART provides a 'field-ready' solution for monitoring GM crops and their interaction with wild plants or non-GM crops." | Genetically Modified | 2,012 |
April 26, 2012 | https://www.sciencedaily.com/releases/2012/04/120426135234.htm | From embryonic stem cells, a sperm replacement and easier path to genetic modification | Researchers reporting in the April 27 issue of the journal | Not only will the advance make it easier to produce genetically modified mice, but it may also enable genetic modification of animals that can't be modified by today's means. The technique might ultimately be used in assisted human reproduction for those affected by genetic disease, the researchers suggest."The current procedure to generate genetically modified animals is tedious and very inefficient," said Jinsong Li of the Shanghai Institute for Biological Sciences. "We thought if we can generate haploid embryonic stem cells and produce semicloned animals by simply injecting those cells into oocytes, we would be certain to get a transmission into offspring with limited breeding as half of the progeny will inherit the genetic modification."Currently, genetically modified mice are made from embryonic stem cells carrying two copies of every gene, one from mom and one from dad. These diploid embryonic cells are injected into blastocysts early in development to produce chimeras, animals whose tissues are made up of cells with one of two genomic identities. As the modified genome is randomly incorporated into the cells that will give rise to eggs and sperm, genetic modifications have the possibility to be passed on to future generations. But it's a slow and uncertain process.Now, Jinsong Li, Guo-Liang Xu and their colleagues have found a way to generate haploid embryonic stem cells (haESCs) that can be used in place of sperm. They produce these specialized cells by first removing the nucleus from immature eggs (oocytes) and then injecting them withsperm. This procedure produces haESCs that partially retain chemical modifications characteristic of the paternal line -- enough that they can be successfully used in place of sperm.The researchers successfully produce live mice bearing haESC-carried genetic traits. These animals, which they call "semicloned mice," grew into fertile adults."By being amenable to gene manipulations and supporting transmission of genetic information to offspring, these haploid cells open new avenues for the generation of genetically modified animals," the researchers write. The next challenge is to improve the sperm-like features of the haESCs by optimizing their makeup without otherwise compromising them.The new method might also lead to genetic modification of animals, such as monkeys, that have been off limits because they don't support the production of chimeras, Li says.As for human reproduction, right now the haESCs are clearly not as good as sperm for the purposes of IVF, but they could someday have advantages. "A similar technique might be one day used to correct genetic disease in germ cells in humans to have a healthy baby for parents," Li said. | Genetically Modified | 2,012 |
April 26, 2012 | https://www.sciencedaily.com/releases/2012/04/120426135010.htm | Manipulating molecules in heart protects mice on high-fat diets from obesity, affects metabolism | UT Southwestern Medical Center researchers have demonstrated for the first time that the heart can regulate energy balance throughout the body, a finding that may point to more effective treatments for obesity, diabetes, and heart disease. | Obesity, cardiovascular disease, and diabetes affect tens of millions of people in the U.S., according to the Centers for Disease Control and Prevention.Using mice fed a high-fat diet, researchers found that manipulating a heart-specific genetic pathway prevents obesity and protects against harmful blood-sugar changes associated with type 2 diabetes. The scientists' findings appear in the April 27 issue of "Obesity, diabetes, and coronary artery disease are major causes of human death and disability, and they are all connected to metabolism. This is the first demonstration that the heart can regulate systemic metabolism, which we think opens up a whole new area of investigation," said Dr. Eric Olson, chairman of molecular biology at UT Southwestern and senior author of the study. Lead author of the Their study used genetically altered mice and an experimental drug to manipulate levels of two regulatory molecules in the heart. The scientists found that MED13, a crucial part of a gene pathway in the heart, controls whole-body metabolism while miRNA-208a, a heart-specific microRNA, inhibits the action of MED13.Mice with MED13 levels that were increased either genetically or by a drug were lean and showed an increase in energy expenditure, the researchers said. In contrast, mice genetically engineered to lack MED13 in the heart showed increased susceptibility to diet-induced obesity. These mice also had aberrant blood-sugar metabolism and other changes similar to those of a group of conditions called metabolic syndrome, which is linked to the development of coronary artery disease, stroke, and type 2 diabetes.MicroRNAs are small snippets of genetic material once considered of little interest because they do not code for the proteins used in body processes the way larger strands of genetic material do. In recent years, these molecules have emerged as key regulators of disease and stress responses in various tissues. At least 500 microRNAs have been identified."Several years ago, our lab focused on this heart-specific microRNA, miR-208a, and then worked with a biotechnology company to develop a drug to inhibit miR-208a. While studying the effects of that drug, we observed that animals treated with the inhibitor seemed to be resistant to high-fat diets but were otherwise healthy," Dr. Olson said. He is one of five co-founders of the biotechnology company, the Colorado-based miRagen Therapeutics Inc., in which UT Southwestern has an equity stake.The current study builds on that original observation by identifying the role of miR-208a and its target MED13 in regulating systemic metabolism. How this heart-specific microRNA communicates with cells throughout the body will be the subject of future studies, Dr. Grueter said.This work was supported, in part, by grants from the National Institutes of Health, the Donald W. Reynolds Center for Clinical Cardiovascular Research, the Robert A. Welch Foundation, the Fondation Leducq-Transatlantic of Excellence in Cardiovascular Research Program, and the American Heart Association-Jon Holden DeHaan Foundation. Dr. Grueter received fellowship support from the American Diabetes Association.Other investigators involved were Brett A. Johnson, a doctoral candidate of molecular biology; Susan DeLeon, graduate student; Lillian Sutherland, senior research scientist; Xiaoxia Qi, research scientist; Dr. Laurent Gautron, instructor of internal medicine; Dr. Joel Elmquist, professor of internal medicine, psychiatry, and pharmacology; Dr. Rhonda Bassel-Duby, professor of molecular biology; and Dr. Eva van Rooij of miRagen Therapeutics. | Genetically Modified | 2,012 |
April 26, 2012 | https://www.sciencedaily.com/releases/2012/04/120426105705.htm | The Generation X report: Food in the lives of GenXers | Generation X adults prepare an average of 10 meals a week, and eat out or buy fast food an average of three times a week, according to a University of Michigan report that details the role food plays in the lives of Americans born between 1961 and 1981. | GenX men are surprisingly involved in shopping for food and cooking, the report shows. They go grocery shopping more than once a week, on average, and cook an average of about eight meals a week -- much more often than their fathers did."I was surprised to see how often GenX men shop and cook," said Jon Miller, author of The Generation X Report. "Women, particularly married women, are still doing more cooking and shopping. But men are much more involved in these activities than they used to be. The stereotype that men can't do much more in the kitchen than boil water just can't hold water, as it were."Using data from about 3,000 young adults collected as part of the ongoing Longitudinal Study of American Youth funded by the National Science Foundation, the report details where GenXers look for information about food, how often they entertain at home and how they feel about organic and genetically modified foods."Food does more than provide necessary sustenance," Miller said. "Meals provide an important time for families to gather together and share their lives, and also mark special occasions with family, friends and neighbors."Food is also a source of concern, according to Miller, and the new report covers GenX attitudes about potential food-related benefits and threats. What kinds of food are healthiest to eat and serve your family? Where should you turn for the best information about potential threats from genetically modified foods?Among the key findings:"In the 21st century, food often involves judgments that may require some scientific understanding," Miller said. "Young adults who are scientifically literate are most able to monitor news about food safety, and most able to identify and use credible sources of information about a topic that directly affects their own health and the health of friends and family." | Genetically Modified | 2,012 |
April 12, 2012 | https://www.sciencedaily.com/releases/2012/04/120412182253.htm | Engineered stem cells seek out and kill HIV in living mice | Expanding on previous research providing proof-of-principle that human stem cells can be genetically engineered into HIV-fighting cells, a team of UCLA researchers have now demonstrated that these cells can actually attack HIV-infected cells in a living organism. | The study, published April 12 in the journal "We believe that this study lays the groundwork for the potential use of this type of an approach in combating HIV infection in infected individuals, in hopes of eradicating the virus from the body," he said.In the previous research, the scientists took CD8 cytotoxic T lymphocytes -- the "killer" T cells that help fight infection -- from an HIV-infected individual and identified the molecule known as the T cell receptor, which guides the T cell in recognizing and killing HIV-infected cells. However, these T cells, while able to destroy HIV-infected cells, do not exist in great enough quantities to clear the virus from the body. So the researchers cloned the receptor and used this to genetically engineer human blood stem cells. They then placed the engineered stem cells into human thymus tissue that had been implanted in mice, allowing them to study the reaction in a living organism.The engineered stem cells developed into a large population of mature, multi-functional HIV-specific CD8 cells that could specifically target cells containing HIV proteins. The researchers also discovered that HIV-specific T cell receptors have to be matched to an individual in much the same way an organ is matched to a transplant patient.In this current study, the researchers similarly engineered human blood stem cells and found that they can form mature T cells that can attack HIV in tissues where the virus resides and replicates. They did so by using a surrogate model, the humanized mouse, in which HIV infection closely resembles the disease and its progression in humans.In a series of tests on the mice's peripheral blood, plasma and organs conducted two weeks and six weeks after introducing the engineered cells, the researchers found that the number of CD4 "helper" T cells -- which become depleted as a result of HIV infection -- increased, while levels of HIV in the blood decreased. CD4 cells are white blood cells that are an important component of the immune system, helping to fight off infections. These results indicated that the engineered cells were capable of developing and migrating to the organs to fight infection there.The researchers did note a potential weakness with the study: Human immune cells reconstituted at a lower level in the humanized mice than they would in humans, and as a result, the mice's immune systems were mostly, though not completely, reconstructed. Because of this, HIV may be slower to mutate in the mice than in human hosts. So the use of multiple, engineered T cell receptors may be one way to adjust for the higher potential for HIV mutation in humans."We believe that this is the first step in developing a more aggressive approach in correcting the defects in the human T cell responses that allow HIV to persist in infected people," Kitchen said.The researchers will now begin making T cell receptors that target different parts of HIV and that could be used in more genetically matched individuals, he said. | Genetically Modified | 2,012 |
March 26, 2012 | https://www.sciencedaily.com/releases/2012/03/120326160651.htm | Tiny reader makes fast, cheap DNA sequencing feasible | Researchers have devised a nanoscale sensor to electronically read the sequence of a single DNA molecule, a technique that is fast and inexpensive and could make DNA sequencing widely available. | The technique could lead to affordable personalized medicine, potentially revealing predispositions for afflictions such as cancer, diabetes or addiction."There is a clear path to a workable, easily produced sequencing platform," said Jens Gundlach, a University of Washington physics professor who leads the research team. "We augmented a protein nanopore we developed for this purpose with a molecular motor that moves a DNA strand through the pore a nucleotide at a time."The researchers previously reported creating the nanopore by genetically engineering a protein pore from a mycobacterium. The nanopore, from Mycobacterium smegmatis porin A, has an opening 1 billionth of a meter in size, just large enough for a single DNA strand to pass through.To make it work as a reader, the nanopore was placed in a membrane surrounded by potassium-chloride solution, with a small voltage applied to create an ion current flowing through the nanopore. The electrical signature changes depending on the type of nucleotide traveling through the nanopore. Each type of DNA nucleotide -- cytosine, guanine, adenine and thymine -- produces a distinctive signature.The researchers attached a molecular motor, taken from an enzyme associated with replication of a virus, to pull the DNA strand through the nanopore reader. The motor was first used in a similar effort by researchers at the University of California, Santa Cruz, but they used a different pore that could not distinguish the different nucleotide types.Gundlach is the corresponding author of a paper published online March 25 by "The motor pulls the strand through the pore at a manageable speed of tens of milliseconds per nucleotide, which is slow enough to be able to read the current signal," Gundlach said.Gundlach said the nanopore technique also can be used to identify how DNA is modified in a given individual. Such modifications, referred to as epigenetic DNA modifications, take place as chemical reactions within cells and are underlying causes of various conditions."Epigenetic modifications are rather important for things like cancer," he said. Being able to provide DNA sequencing that can identify epigenetic changes "is one of the charms of the nanopore sequencing method."Coauthors of the Nature Biotechnology paper are Elizabeth Manrao, Ian Derrington, Andrew Laszlo, Kyle Langford, Matthew Hopper and Nathaniel Gillgren of the UW, and Mikhail Pavlenok and Michael Niederweis of the University of Alabama at Birmingham.The work was funded by the National Human Genome Research Institute in a program designed to find a way to conduct individual DNA sequencing for less than $1,000. When that program began, Gundlach said, the cost of such sequencing was likely in the hundreds of thousands of dollars, but "with techniques like this it might get down to a 10-dollar or 15-minute genome project. It's moving fast." | Genetically Modified | 2,012 |
March 26, 2012 | https://www.sciencedaily.com/releases/2012/03/120326112504.htm | E. coli bacteria becomes factory for sugar-modified proteins to make cheaper, faster pharmaceuticals | Escherichia coli -- a bacteria considered the food safety bane of restaurateurs, grocers and consumers -- is a friend. Cornell University biomolecular engineers have learned to use | Matthew DeLisa, Cornell associate professor of chemical and biomolecular engineering, and his research team, now have published a novel method for engineering human therapeutic glycoproteins simply and quickly by using Glycoproteins are proteins that are modified at specific amino acid "acceptor" sites with complex carbohydrate structures, or oligosaccharides -- a basic human chemical reaction that's essential to life. That's why specifically designed, genetically engineered glycoproteins are so commonly used as drugs -- they bind to certain protein receptor sites and, for example, block cancer cells from multiplying. Among glycoproteins used to treat diseases today are monoclonal antibodies and interferons.Current manufacturing methods rely mainly on costly, time-consuming mammalian culture cells, such as the Chinese Hamster Ovary (CHO) cell line. The process is also susceptible to viral contamination, further driving up production cost. In fact in 2009, another biopharmaceutical company temporarily shut down its plant after such a contamination occurred.The Cornell research uses a method to assemble a synthetic pathway for the simple and quick production of a glycoprotein that forms the basis of many of today's therapeutic protein drugs, including, for example, the protein GCase, used in a drug that treats Gaucher's disease. To do so, they artificially introduced the machinery of glycosylation -- the chemical process by which proteins become glycoproteins -- into The synthetic pathway they designed, which can be tailored to many amino acid acceptor sites to make different drugs, starts with native enzymes in DeLisa and his colleagues are now working to improve their approach that they call "glycans by design" -- using the enzyme-based protein production method to specifically tailor sugar structures to make many different glycans and glycoproteins.The National Institutes of Health, the National Science Foundation, and the New York State Office of Science, Technology and Academic Research funded the work. | Genetically Modified | 2,012 |
March 23, 2012 | https://www.sciencedaily.com/releases/2012/03/120323134535.htm | Who knew? Fruit flies get kidney stones too | Research on kidney stones in fruit flies may hold the key to developing a treatment that could someday stop the formation of kidney stones in humans, a team from Mayo Clinic and the University of Glasgow found. | They recently presented their findings at the Genetics Society of America annual meeting."The kidney tubule of a fruit fly is easy to study because it is transparent and accessible," says physiologist Michael F. Romero, Ph.D., of Mayo Clinic in Rochester, Minn. He said researchers are now able to see new stones at the moment of formation."More important is that fruit flies are not bothered by the presence of kidney stones, so they are ideal subjects to study in order to better understand the condition in humans," Dr. Romero says.For example, Dr. Romero's team has identified a gene that encodes a protein which transports oxalate into the fly kidney. When this gene is genetically modified, flies get fewer stones.Dr. Romero and his colleagues are now using this gene as a target as they test gut, renal and crystal dissolving therapies in fruit flies for possible drug development."Our hope is that, by using a relatively inexpensive and flexible disease model like | Genetically Modified | 2,012 |
March 19, 2012 | https://www.sciencedaily.com/releases/2012/03/120319194313.htm | Scientists develop tools to make more complex biological machines from yeast | Scientists are one step closer to making more complex microscopic biological machines, following improvements in the way that they can "re-wire" DNA in yeast, according to research recently published in the journal | The researchers, from Imperial College London, have demonstrated a way of creating a new type of biological "wire," using proteins that interact with DNA and behave like wires in electronic circuitry. The scientists say the advantage of their new biological wire is that it can be re-engineered over and over again to create potentially billions of connections between DNA components. Previously, scientists have had a limited number of "wires" available with which to link DNA components in biological machines, restricting the complexity that could be achieved.The team has also developed more of the fundamental DNA components, called "promoters," which are needed for re-programming yeast to perform different tasks. Scientists currently have a very limited catalogue of components from which to engineer biological machines. By enlarging the components pool and making it freely available to the scientific community via rapid Open Access publication, the team in this new study aims to spur on development in the field of synthetic biology.Future applications of this work could include tiny yeast-based machines that can be dropped into water supplies to detect contaminants, and yeast that records environmental conditions during the manufacture of biofuels to determine if improvements can be made to the production process.Dr Tom Ellis, senior author of the paper from the Centre for Synthetic Biology and Innovation and the Department of Bioengineering at Imperial College London, says: "From viticulture to making bread, humans have been working with yeast for thousands of years to enhance society. Excitingly, our work is taking us closer to developing more complex biological machines with yeast. These tiny biological machines could help to improve things such as pollution monitoring and cleaner fuels, which could make a difference in all our lives."Dr Benjamin Blount, first author of the paper from the Centre for Synthetic Biology and Innovation and the Department of Bioengineering at Imperial College London, says: "Our new approach to re-wiring yeast opens the door to an exciting array of more complex biological devices, including cells engineered to carry out tasks similar to computers."In the study, the Imperial researchers modified a protein-based technology called TAL Effectors, which produce TALOR proteins, with similar qualities to wires in electronic devices. These TALORS can be easily re-engineered, which means that they can connect with many DNA-based components without causing a short circuit in the device.The team says their research now provides biological engineers working in yeast with a valuable new toolbox.Professor Richard Kitney, Co-Director of the Centre for Synthetic Biology and Innovation at the College, adds: "The work by Dr Ellis and the team at the Centre really takes us closer to developing much more complex biological machines with yeast, which may help to usher in a new age where biological machines could help to improve our health, the way we work, play and live."Professor Paul Freemont, Co-Director of the Centre for Synthetic Biology and Innovation at the College, concludes: "One of the core aims of the Centre is to provide tools and resources to the wider scientific community by sharing our research. Dr Ellis's team has now begun to assemble characterised biological parts for yeast that will be available to researchers both in academia and industry." | Genetically Modified | 2,012 |
March 19, 2012 | https://www.sciencedaily.com/releases/2012/03/120319094801.htm | The Viking journey of mice and men | House mice ( | During the Viking age (late 8th to mid 10th century) Vikings from Norway established colonies across Scotland, the Scottish islands, Ireland, and Isle of Man. They also explored the north Atlantic, settling in the Faroe Islands, Iceland, Newfoundland and Greenland. While they intentionally took with them domestic animals such as horses, sheep, goats and chickens they also inadvertently carried pest species, including mice.A multinational team of researchers from the UK, USA, Iceland, Denmark and Sweden used techniques designed to characterize genetic similarity, and hence the relatedness of one population, or one individual, with another, to determine a mouse colonization timeline. Modern samples of mouse DNA were collected and compared to ancient samples dating mostly from the 10th to the 12th century. Samples of house mouse DNA were collected from nine sites in Iceland, Narsaq in Greenland, and four sites near the Viking archaeological site, L'Anse aux Meadows, in Newfoundland. The ancient samples came from the Eastern and Western settlements in Greenland and four archaeological sites in Iceland.Analysis of mouse mitochondrial DNA showed that house mice (Dr Eleanor Jones (affiliated with the University of York and Uppsala University) explained, "Human settlement history over the last 1000 years is reflected in the genetic sequence of mouse mitochondrial DNA. We can match the pattern of human populations to that of the house mice." Prof Jeremy Searle, from Cornell University, continued, "Absence of traces of ancestral DNA in modern mice can be just as important. We found no evidence of house mice from the Viking period in Newfoundland. If mice did arrive in Newfoundland, then like the Vikings, their presence was fleeting and we found no genetic evidence of it." | Genetically Modified | 2,012 |
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