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    News

    CoyoteRidge-630With estimates of losing 15 to 40 percent of the world's species over the next four decades – due to climate change and habitat loss, researchers ponder in the Sept. 26 issue of Nature whether science should employ genetic engineering to the rescue.
    The technique would involve "rescuing a target population or species with adaptive alleles, or gene variants, using genetic engineering," write Josh Donlan, Cornell visiting fellow in ecology and evolutionary biology, and his colleagues. The method is "an increasingly viable … option, which we call 'facilitated adaptation,' [but it] has been little discussed," they add.
    To avert mass extinctions, the group thinks that three options, each with its own set of challenges, complications and risks, exist. They are:

    - Animals or plants could be crossed with individuals of the same species from better-adapted populations to introduce adapted alleles into threatened animal or plant populations.

    - Direct transfers from populations with adapted genomes could be introduced into the threatened populations of the same species.

    - Genes from a well-adapted species could be incorporated into the genomes of endangered species.

    The Nature commentary draws from a recent National Science Foundation-funded workshop, "Ecological and Genomic Exploration of Environmental Change," in March, where scientists met to understand issues surrounding climate change adaptation. In those spirited discussions, a hot question emerged: Is managed relocation of animal and plant species really the only approach to averting extinction? Instead of moving plant and animal populations, could genes be moved into populations? "Thus, the term 'facilitated adaptation' was born," said Donlan.
    Averting climate change altogether would be a preferable – albeit unlikely – outcome. The scientists fear that implementing genetic solutions could potentially deter other climate change action.
    "A serious concern is that even the possibility of using genetic-engineering tools to rescue biodiversity will encourage inaction with regard to climate change. Before genetic engineering can be seriously entertained as a tool for preserving biodiversity, conservationists need to agree on the types of scenario for which facilitated adaptation, managed relocation and other adaptation strategies might be appropriate, and where such strategies are likely to fail or introduce more serious problems," they write.
    Joining Donlan on the Nature commentary, "Gene Tweaking for Conservation," are Michael A. Thomas, Idaho State University, first and corresponding author; Gary W. Roemer, New Mexico State University, Las Cruces, N.M.; Brett G. Dickson, Conservation Science Partners, Truckee, Calif.; and Marjorie Matocq and Jason Malaney, University of Nevada, Reno. Donlan is also executive director of the Advanced Conservation Strategies, Midway, Utah.

    newroleforprPioneering new research from a team of Indiana University Bloomington biologists has shown for the first time that a protein which has been long known to be critical for the initiation of protein synthesis in all organisms can also play a role in the regulation of gene expression in some bacteria, and probably land plants as well.
    The protein, called translation initiation factor 3, or IF3, is one of three proteins that make up the core structure of the machinery needed to guide the joining of messenger RNAs and ribosomes as protein translation commences. These three proteins have been widely considered to simply operate in a constitutive manner and play little, if any, role in regulating the expression of genes.
    The new findings, from the laboratory of David M. Kehoe, professor of biology in the Indiana University Bloomington College of Arts and Sciences, reveals that IF3, in addition to its well-accepted function during translation initiation, also regulates the expression of genes that encode components of the photosynthetic machinery in response to changes in the color of light in the surrounding environment, a process known as "chromatic acclimation."
    These photosynthesis genes produce red-pigmented proteins called phycoerythrin in cyanobacteria when the cells are grown in green light and allow these organisms to efficiently absorb the predominant ambient light color for photosynthesis. The team uncovered the novel function of IF3 while searching for mutants that incorrectly regulated phycoerythrin. The discovery of this mutant was at first surprising, because in all other bacteria that have been examined, mutations in infC (the gene that encodes IF3) are lethal.
    The team solved this puzzle by uncovering a second infC gene in Fremyella diplosiphon, the model organism for the study of light color responsiveness in cyanobacteria. While both IF3s, which have been named IF3a and IF3b, can act in the traditional role of translation initiation, only IF3a was found to also regulate photosynthetic gene expression.
    By exploring the genomes of hundreds of prokaryotes and eukaryotes in collaboration with members of the laboratory of Indiana University Distinguished Professor and Class of 1955 Professor Jeffrey Palmer, the group identified a wide range of species whose genomes appear to have the potential to encode multiple IF3s, with one organism apparently encoding five distinct IF3 family members. And since almost none of these species are capable of chromatic acclimation, Kehoe believes that multiple IF3s must be used to regulate a wide range of environmental and perhaps developmental responses in both prokaryotes and eukaryotes.
    "Particularly interesting was our finding that IF3 families exist in a number of plant species, including commercially important crops," Kehoe said. "This means that new approaches to the modification of traits in agriculturally significant plant species may be possible by manipulating the expression patterns of different IF3 family members."
    The discovery has generated excitement for an additional reason. Historically, scientists have had a difficult time studying IF3 because it is so essential for translation initiation that it can not be altered without causing death. In fact, it remains one of the few proteins involved in translation for which no effective antibiotic has been developed. But the ability of the Kehoe team to delete either of the two infC genes in F. diplosiphon without causing lethality will allow the group to modify both IF3a and IF3b at will.
    "Now that we know that F. diplosiphon contains two functionally different IF3s, and that each is nonessential, we have a unique opportunity to enhance our understanding of how the structural features of IF3 are related to its function," Kehoe said. "Advancing our understanding of the role of IF3 in translation is likely to provide opportunities to develop new antibiotics that are targeted to this class of proteins."
    "A unique role for translation initiation factor 3 in the light color regulation of photosynthetic gene expression" is now available in early online editions of the Proceedings of the National Academy of Sciences. Co-authors with Kehoe and Palmer were Andrian Gutu, a former Ph.D. student in the Kehoe lab who is now a Howard Hughes Medical Institute Postdoctoral Fellow at Harvard University; April Nesbit, a former postdoctoral researcher in the Kehoe lab who is now a lecturer at Purdue Northwest; and Andrew Alverson, a former postdoctoral fellow in the Palmer lab who is now a faculty member at the University of Arkansas. Primary funding for the work was provided by the National Science Foundation, with support provided to Nesbit by the National Institutes of Health.

    toxoplasmainChronic infection with the parasite Toxoplasma gondii can make mice lose their innate, hard-wired fear of cats. This loss of their innate fear may persist after the parasite is no longer detectable in their brains, suggesting that initial infection may cause permanent changes in the mechanisms underlying their fear of predators. The results are published September 18 in the open access journal PLOS ONE by Wendy Ingram and colleagues from the University of California, Berkeley.
    The Toxoplasma parasite can be deadly, causing spontaneous abortion in pregnant women or killing immune-compromised patients, but it has even stranger effects in mice.
    Infected mice lose their fear of cats, which is good for both cats and the parasite, because the cat gets an easy meal and the parasite gets into the cat's intestinal track, the only place it can sexually reproduce and continue its cycle of infection.
    New research by graduate student Wendy Ingram at the University of California, Berkeley, reveals a scary twist to this scenario: the parasite's effect seem to be permanent. The fearless behavior in mice persists long after the mouse recovers from the flu-like symptoms of toxoplasmosis, and for months after the parasitic infection is cleared from the body, according to research published today (Sept. 18) in the journal PLOS ONE.
    "Even when the parasite is cleared and it's no longer in the brains of the animals, some kind of permanent long-term behavior change has occurred, even though we don't know what the actual mechanism is," Ingram said. She speculated that the parasite could damage the smell center of the brain so that the odor of cat urine can't be detected. The parasite could also directly alter neurons involved in memory and learning, or it could trigger a damaging host response, as in many human autoimmune diseases.
    Ingram became interested in the protozoan parasite, Toxoplasma gondii, after reading about its behavior-altering effects in mice and rats and possible implications for its common host, the domesticated cat, and even humans. One-third of people around the world have been infected with Toxoplasma and probably have dormant cysts in their brains. Kept in check by the body's immune system, these cysts sometimes revive in immune-compromised people, leading to death, and some preliminary studies suggest that chronic infection may be linked to schizophrenia or suicidal behavior.

    Pregnant women are already warned to steer clear of kitty litter, since the parasite is passed through cat feces and can cause blindness or death in the fetus. One main source of spread is undercooked pork, Ingram said.
    With the help of Michael Eisen and Ellen Robey, UC Berkeley professors of molecular and cell biology, Ingram set out three years ago to discover how Toxoplasma affects mice's hard-wired fear of cats. She tested mice by seeing whether they avoided bobcat urine, which is normal behavior, versus rabbit urine, to which mice don't react. While earlier studies showed that mice lose their fear of bobcat urine for a few weeks after infection, Ingram showed that the three most common strains of Toxoplasma gondii make mice less fearful of cats for at least four months.
    Using a genetically altered strain of Toxoplasma that is not able to form cysts and thus is unable to cause chronic infections in the brain, she demonstrated that the effect persisted for four months even after the mice completely cleared the microbe from their bodies. She is now looking at how the mouse immune system attacks the parasite to see whether the host's response to the infection is the culprit.
    "This would seem to refute – or at least make less likely – models in which the behavior effects are the result of direct physical action of parasites on specific parts of the brain," Eisen wrote in a blog post about the research.
    "The idea that this parasite knows more about our brains than we do, and has the ability to exert desired change in complicated rodent behavior, is absolutely fascinating," Ingram said. "Toxoplasma has done a phenomenal job of figuring out mammalian brains in order to enhance its transmission through a complicated life cycle."

    13-researchersc-gene-targeting-rosa26-feeder-cells-human-primary-cells-mef cells-rat

    A computational model developed by researchers at Rensselaer Polytechnic Institute is the first to accurately simulate the complex twists of a short sequence of RNA as it folds into a critical hairpin structure known as a "tetraloop." The research, published today in Proceedings of the National Academy of Sciences, is a glimpse into RNA, found in all life on Earth, and could advance a variety of research areas, including the search for new antibiotics and cures for protein-related diseases.
    Existing computational models, based on DNA rather than RNA, do not achieve the atomic level accuracy of the new model, said Angel Garcia, head of the Department of Physics, Applied Physics, and Astronomy within the School of Science at Rensselaer, and senior constellation chaired professor in the Biocomputation and Bioinformatics Constellation, who co-wrote the paper with Alan Chen, a post-doctoral fellow at Rensselaer. The new model Garcia and Chen created can simulate the folding of three known versions of a tetraloop, accurate to within one ten-billionth of a meter.
    RNA is involved in many biological functions, such as building proteins, coding and decoding genes, and cellular regulation. RNA molecules are composed of strings of four different "bases" —cytosine, guanine, adenine, and uracil—mounted on a sugar-phosphate backbone. Once the sequence is assembled, the individual bases interact with their neighbors, twisting and swinging on the hinged chemical bonds that connect them to the backbone. When the process is complete, the RNA has folded into its "tertiary" structure, which influences its function. Although researchers can easily alter the sequence of molecules, without accurate computer modeling there they cannot easily see the tertiary structure of their creation.
    "Right now, it takes people from molecular biologists, to virologists, to cell biologists, thousands of dollars and years of study to see the structure of an RNA they have made, altered, or are studying," said Chen. "There are a lot of researchers working on the RNA in viruses and how it attacks the cell, and, while they're easily able to alter the sequence, they're essentially working without ever seeing the effects of their changes in molecular detail. Because of this, there's a lot of trial and error, and our work aimed at helping that."
    Garcia and Chen said that, unlike DNA, which typically twists two strands of bases into a classic double-helix, RNA is single-stranded and folds onto itself, forming many unusual structures. A tetraloop is a small section of single-stranded RNA that is looped into the shape of a hairpin, the curve of which is formed by four bases. Even the sequence of bases in a tetraloop is unusual, violating a standard arrangement described by groundbreaking DNA researchers James Watson and Francis Crick.
    To create an effective computational model, Garcia and Chen had to match the unique "recipe" of twisting and swinging proscribed by the interactions between the bases.
    "Imagine if you try to produce a recipe of Mario Batali," said Garcia, referring to a popular chef. "I tell you it has water, salt, fish, and pasta—go produce his recipe. The problem is, you don't know how much of each, and in what order."
    Instead of a recipe of food ingredients, Garcia and Chen created a computational recipe for the interactions of the bases in the sequence of a tetraloop.
    "The problem is one of balancing different forces. It's the actions between the bases as they stack on top of each other, the interactions of the bases with water, the rotation of the bases relative to a sugar. Those are things that change the balance," said Garcia.
    Garcia said tetraloops are an important area of study because they appear in all organisms, particularly in ribosomes, which manufacture proteins for living cells. Statistically, there could be as many as 256 possible sequences of those four bases, but only three sequences actually appear in tetraloops. Once formed, they are highly stable, outlasting other structures when subjected to the destructive force of increasing heat.
    "Tetraloops are sequences which are highly conserved throughout evolution; you find them everywhere, from bacteria to humans," said Garcia. "From one organism to another, many things can change, but when tetraloops change, they change from one sequence of four bases to one of the other three. They stack against each other and they are hyperstable. And there is a reason for them to be arranged the way they are."

    4950664-3x2-940x627-neural-stem-cells-rat-models-gene-targeting-rosa26-feeder-cells-human-primary-cellsModern technology will allow you to avoid repetitive operations to remove the rest of the tumor.

    Inventors at the University of Western Australia presented the world's smallest portable microscope. It is adapted for the detection of cancerous cells, showing the three-dimensional images. The basic element of the invention is a lens, whose width is one-third of a millimeter, and so it easily fits into the needle.

    Currently new technology passes tests on samples of human tissue. A successful will allow you to avoid repetitive operations to remove the rest of the tumor. According to statistics, nearly one in four women, operated by breast cancer undergoes re-intervention.

    The microscope is set to be used during the operation, which will help to be examined within the tumor. It will also be possible to examine the operation of the lungs in emphysema and cancer of the brain. If the tests pass, the advanced technology could hit the market over the next ten years.

    Thursday, 12 September 2013 11:26

    The Secret Lives (and Deaths) of Neurons

    As the human body fine-tunes its neurological wiring, nerve cells often must fix a faulty connection by amputating an axon -- the "business end" of the neuron that sends electrical impulses to tissues or other neurons. It is a dance with death, however, because the molecular poison the neuron deploys to sever an axon could, if uncontained, kill the entire cell.

    Researchers from the University of North Carolina School of Medicine have uncovered some surprising insights about the process of axon amputation, or "pruning," in a study published May 21 in the journal Nature Communications. Axon pruning has mystified scientists curious to know how a neuron can unleash a self -destruct mechanism within its axon, but keep it from spreading to the rest of the cell. The researchers' findings could offer clues about the processes underlying some neurological disorders.

    "Aberrant axon pruning is thought to underlie some of the causes for neurodevelopmental disorders, such as schizophrenia and autism," said Mohanish Deshmukh, PhD, professor of cell biology and physiology at UNC and the study's senior author. "This study sheds light on some of the mechanisms by which neurons are able to regulate axon pruning."

    Axon pruning is part of normal development and plays a key role in learning and memory. Another important process, apoptosis -- the purposeful death of an entire cell -- is also crucial because it allows the body to cull broken or incorrectly placed neurons. But both processes have been linked with disease when improperly regulated.

    The research team placed mouse neurons in special devices called microfluidic chambers that allowed the researchers to independently manipulate the environments surrounding the axon and cell body to induce axon pruning or apoptosis.

    They found that although the nerve cell uses the same poison -- a group of molecules known as Caspases -- whether it intends to kill the whole cell or just the axon, it deploys the Caspases in a different way depending on the context.

    "People had assumed that the mechanism was the same regardless of whether the context was axon pruning or apoptosis, but we found that it's actually quite distinct," said Deshmukh. "The neuron essentially uses the same components for both cases, but tweaks them in a very elegant way so the neuron knows whether it needs to undergo apoptosis or axon pruning."

    In apoptosis, the neuron deploys the deadly Caspases using an activator known as Apaf-1. In the case of axon pruning, Apaf-1 was simply not involved, despite the presence of Caspases. "This is really going to take the field by surprise," said Deshmukh. "There's very little precedent of Caspases being activated without Apaf-1. We just didn't know they could be activated through a different mechanism."

    In addition, the team discovered that neurons employ other molecules as safety brakes to keep the "kill" signal contained to the axon alone. "Having this brake keeps that signal from spreading to the rest of the body," said Deshmukh. "Remarkably, just removing one brake makes the neurons more vulnerable."

    Deshmukh said the findings offer a glimpse into how nerve cells reconfigure themselves during development and beyond. Enhancing our understanding of these basic processes could help illuminate what has gone wrong in the case of some neurological disorders.

    M Id 416855 J-assay-kits-cell-monoclonal-polyclonal-peptide-biological-research-products

    If the gene has a similar role in humans will be able to develop new screening tests

    British scientists have identified a gene in mice, which increases the risk of ovarian cancer, as defective.

    Rodents lacking gene are twice as likely to develop cancer, ovarian cancer, and to show signs of infertility. If the gene has a similar role in humans will be able to develop new screening tests, said scientists from the charity Cancer Research UK.

    They focus on gene Helq, who was involved in the restoration of damaged DNA. It turned out that mice deprived of it, are two-fold higher risk of ovarian cancer.

    "The results show that if there are problems with Helq in mice increases the likelihood of developing ovarian cancer and other tumors, said study leader Dr. Simon Boultan. This is exciting because it is possible the same effect was observed in women with a defective gene Helq. The next step is to check whether this is so."

    Zebrafish with very weak muscles helped scientists decode the elusive genetic mutation responsible for Native American myopathy, a rare, hereditary muscle disease that afflicts Native Americans in North Carolina.

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    Scientists led by John Kuwada, professor of molecular, cellular and developmental biology at the University of Michigan, and Hiromi Hirata of the National Institute of Genetics in Japan originally identified the gene in mutant zebrafish that exhibited severe muscle weakness. Native American myopathy causes muscle weakness from birth and other severe problems that can lead to death before adulthood.

    The findings appear in the journal Nature Communications.

    The responsible gene encodes for a muscle protein called Stac3, which in turn regulates a physiological process required for muscle contraction. The muscles of zebrafish and people with the genetic mutation don't make normal Stac3 protein and the muscles don't contract effectively.

    Scientists established the importance of Stac3 for muscle function in zebrafish by studying the small fish physiologically and genetically. Scientists then looked at the human version of the gene, and found that the gene was mutated in people suffering from Native American myopathy.

    For many degenerative muscle diseases few drugs help, largely because scientists don't know the genes responsible for many of these muscle diseases, making it difficult to develop drugs and other therapies that target the condition. The discovery of the gene for Native American myopathy, however, may help develop drugs to treat the myopathy, as well as other related muscle diseases.

    13338 influenzaMicroneedles is a medium for supply of influenza vaccine, which avoids the pain associated with conventional needles. They are only seven tenths of a millimeter, and the volume of vaccine - an essential factor in pain - is small.
    Instead of liquid, whole killed or attenuated viruses, using dry vaccines virus-like particles (VLPs) that simply coating the needles in the presence of the basic stabilizer, eliminating the need for cooling - the possible handover for use in developing countries.The lower dose required when using microneedles also reduces the potential for side effects, such as lung inflammation.
    "This method can induce higher levels of IgG2a antibody and quick recall to elicit an immune response to infection lethal. Our previous studies showed that the microneedle vaccination enhances antibody-producing cells in the spleen and bone marrow induced compared to intramuscular vaccination" says Sang Moo Kang Georgia State University, researcher of the study.
    Previous studies by this group has shown that an influenza VLP-coated microneedles indeed produce higher short-term protection than traditional intramuscular immunization. In this study, researchers tested how effective long-term protection of the vaccine. Mice that received the vaccine were 100 percent protected against a lethal challenge with influenza virus 14 months after vaccination.
    Kang says that his goal was to develop a simple and painless method of administration of vaccines. He also says that the patient would probably use this system to be vaccinated.

    Soy-protein-shows-brain-boosting-benefits-Human

    Stress protein genetically linked to depression, anxiety and other mental disorders contributes to accelerate Alzheimer chorobyNová study by researchers at the University of South Florida conducted found.

    The study is published online today in the Journal of Clinical Investigation.

    If the voltage protein FKBP51 cooperates with another protein known as Hsp90 chaperone protein is a huge complex prevents distance from the brain of toxic tau protein associated with Alzheimer's disease.

    Under normal circumstances tau helps form the skeleton of our brain cells. USF study was conducted experiments tubes, mice genetically modified to produce abnormal tau protein accumulates in the brains of people with Alzheimer's disease, and Alzheimer's disease post-mortem human brain tissue.

    Researchers reported that FKBP51 levels associated with age in the brain, and pakstres protein Hsp90 are with partners to tau more deadly brain cells in memory formation.

    JeAsistent Hsp90 protein, which monitors the activity of Tau in nerve cells. Chaperone proteins are generally help to ensure that tau proteins are folded properly maintain healthy structure of nerve cells.

    But as FKBP51 levels increase with age, but tear Hsp90 positive impact on the toxicity of tau to promote.

    "We found that Hsp90 FKB51 confiscated environment that prevents removal of dew and allows you to create toxic" said the study's principal investigator Chad Dickey, PhD, professor of molecular medicine at the Institute of USF Health Byrd Alzheimer's disease. "Basically, it is used for the production of Hsp90 and to keep the villain."

    The authors conclude ževývoj drugs or other ways to reduce FKB51 or block their interaction with Hsp90 as a very significant impact on the treatment of tau pathology in Alzheimer's disease, Parkinson's disease, dementia and other diseases associated with more memory loss.

    Earlier studies Dr. Dickey and his colleagues found that a lack of FKBP51 in old mice resistance be improved depressive behavior.