tag:blogger.com,1999:blog-43052834078056262982024-03-22T01:15:52.202-07:00Molecular Biology & Genetics, News & Press - A Blog by Fausto Intilla (WWW.OLOSCIENCE.COM)olosciencehttp://www.blogger.com/profile/07007258673266741468noreply@blogger.comBlogger246125tag:blogger.com,1999:blog-4305283407805626298.post-81881488047638577772015-05-27T08:13:00.001-07:002015-05-27T08:13:11.957-07:00Cooperation among viral variants helps hepatitis C survive immune system attacks. <table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody>
<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEj0uOXp8PE5C3WVhOts592_Bd2-lkkJG2lpOazW22_nsNE5KK7jXrCjINDnn9IRfoupEuNfAJGtOxkLC1ySQbBeO0d-5kAIVnvzIujjV4dm3bs5szu4C9mfcsEdvw8cpOpaofrDREtQRiI/s1600/cooperationa.jpg" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" height="192" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEj0uOXp8PE5C3WVhOts592_Bd2-lkkJG2lpOazW22_nsNE5KK7jXrCjINDnn9IRfoupEuNfAJGtOxkLC1ySQbBeO0d-5kAIVnvzIujjV4dm3bs5szu4C9mfcsEdvw8cpOpaofrDREtQRiI/s320/cooperationa.jpg" width="320" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;">Graph shows a cross-immunoreactivity network (CRN) composed of 100 viral variants. Altruistic variants are shown in green, persistent variants in red, and others in yellow. Credit: Georgia Tech/CDC </td></tr>
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Source: <a href="http://medicalxpress.com/news/2015-05-cooperation-viral-variants-hepatitis-survive.html"><span style="color: yellow;">Phys.org</span></a></div>
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Warring armies use a variety of tactics as they struggle to gain the upper hand. Among their tricks is to attack with a decoy force that occupies the defenders while an unseen force launches a separate attack that the defenders fail to notice.<br />
A study published earlier this month in the journal <i>Proceedings of the National Academy of Sciences</i> suggests that the Hepatitis C virus (HCV) may employ similar tactics to distract the body's natural defenses. After infecting patients, Hepatitis C evolves many variants, among them an "altruistic" group of viral particles that appears to sacrifice itself to protect other mutants from the body's immune system.<br />
The findings, reported by researchers from the Georgia Institute of Technology and the Centers for Disease Control and Prevention (CDC), could help guide development of future vaccines and treatments for the virus, which affects an estimated 170 million people in the world. Developing slowly over many years and often without symptoms, Hepatitis C can cause severe liver damage and cancer. There are currently no vaccines for the disease.<br />
"The members of viral populations in Hepatitis C don't act like separate entities; the different variants work together almost like a team," said Leonid Bunimovich, a Regent's Professor in the Georgia Tech School of Mathematics. "There is a clear separation of responsibilities, including variants we call 'altruistic' because they sacrifice themselves for the good of the whole viral population. These variants seem to draw the immune system attack on themselves."<br />
The findings resulted from mathematical modeling done by the scientists, who first developed a model for how the virus variants and immune system antibodies interact. They then used the model to analyze and explain data gathered from a group of patients infected with Hepatitis C, some of whom had been followed for as long as 20 years.<br />
The virus evolves differently in each person, producing a mix of genetically-related variants over time, Bunimovich noted. Ultimately, the virus variants and the antibodies form a complex network in which an antibody to one variant can react to another variant - a phenomenon known as cross-immunoreactivity.<br />
But how do viruses, which lack brains or even neural cells, produce a level of teamwork that's often difficult for humans to achieve?<br />
"The virus variants do not communicate directly with one another, but in this system of viruses and antibodies, they interact through the antibodies," explained Bunimovich. "When one antibody-producing cell responds to one variant, and then to another, that is a form of interaction that affects both variants. An indirect interaction occurs when the virus variants interact with the same antibody in the network."<br />
Unlike HIV - to which it is often compared - Hepatitis C virus doesn't suppress the body's immune system. Many scientists believe that the viral infection evolves like an "<a class="textTag" href="http://medicalxpress.com/tags/arms+race/" rel="tag">arms race</a>," with the virus mutating to stay one step ahead of the body's immune system. Using next-generation gene sequencing data, the research team - which included regular fellow Pavel Skums and microbiologist Yury Khudyakov from the CDC's Division of Viral Hepatitis - analyzed viral populations in detail. The scientists studied the genetic compositions of the populations, and even saw evolution in blood samples taken from the same persons over time.<br />
The populations of variants rose and fell, some remaining in small numbers and others reappearing after they had been seemingly wiped out by the immune system. At late stages of the persistent infection development, the evolution of new variations almost stopped, though the immune system remained strong. The "arms race" theory fails to explain these observations, Bunimovich said.<br />
Using their model to track both variants and antibodies, the researchers found that certain variants were drawing the <a class="textTag" href="http://medicalxpress.com/tags/immune+system+response/" rel="tag">immune system response</a> on themselves to protect others. They called this newly-observed phenomenon "antigenic cooperation." The antibodies suppressed only the altruistic variants, leaving other viral members of the network unharmed.<br />
"The altruistic variants allow the antibodies to attack them, thereby sacrificing themselves, so other variants can survive," said Skums, the paper's first author. "The altruistic variants fool the immune system, rendering the immune system response to other variants ineffective. In essence, the surviving variants use the altruistic (sacrificing) variants as an umbrella to protect themselves."<br />
The researchers were surprised by the sophisticated behavior, which occurs because the viral variants are part of the complex interconnected network - a social network not unlike the ones created in such environments as Facebook.<br />
"Even such simple organisms as viruses can organize into a network," Skums explained. "Because they are part of a network, they can develop this kind of complex behavior, fighting the <a class="textTag" href="http://medicalxpress.com/tags/immune+system/" rel="tag">immune system</a> through team efforts."<br />
The findings, if supported by additional research, could alter the strategy for developing vaccines for Hepatitis C. Both vaccines and treatment would have to take into account how the virus evolves differently in individuals. The researchers also hope to examine the activity of other viruses to see if this complex interaction may also be found in other viral networks, Bunimovich said.<br />
For the researchers, mathematics allowed them to see patterns that might otherwise have remained hidden in the complex patient data.<br />
"Now that we see this from the mathematical model, everything makes sense," said Skums. "When you look at this mathematically, you can see the whole picture."<br />
<div class="relevant-link">
<a href="http://medicalxpress.com/news/2015-05-cooperation-viral-variants-hepatitis-survive.html#"><img alt="" class="toolsicon ic-rel" height="16" src="http://cdn.medicalxpress.com/tmpl/v5/img/1x1.gif" width="16" /></a> <b>Explore further:</b> <a href="http://phys.org/news/2015-05-sequencing-technique-unveiling-realm-viral.html#inlRlv" itemprop="relatedLink">Sequencing technique unveiling the realm of viral mutations</a> </div>
<b>More information:</b> "Antigenic cooperation among intrahost HCV variants organized into a complex network of cross-immunoreactivity," <i>Proceedings of the National Academy of Sciences</i>, published ahead of print May 4, 2015. <a href="http://www.dx.doi.org/10.1073/pnas.1422942112">www.dx.doi.org/10.1073/pnas.1422942112</a>olosciencehttp://www.blogger.com/profile/07007258673266741468noreply@blogger.com2tag:blogger.com,1999:blog-4305283407805626298.post-14581669478778622992014-10-03T00:17:00.002-07:002014-10-03T00:17:46.849-07:00Geneticists solve 40-year-old dilemma to explain why duplicate genes remain in the genome. <table align="center" cellpadding="0" cellspacing="0" class="tr-caption-container" style="margin-left: auto; margin-right: auto; text-align: center;"><tbody>
<tr><td style="text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEi8JxoJUBg-mivoHv8Hfptsineybc7kte981uY6pwCBUJy93KyeagV511k2dSxQ0xIYC_L0ilprkcMVfKCzHxSXZt7tft2t9AUBqwo_mgZedLYvkDVOdX8W9wxLYfV0VnCjHl7FLuvuiRs/s1600/geneticistss.jpg" imageanchor="1" style="margin-left: auto; margin-right: auto;"><img border="0" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEi8JxoJUBg-mivoHv8Hfptsineybc7kte981uY6pwCBUJy93KyeagV511k2dSxQ0xIYC_L0ilprkcMVfKCzHxSXZt7tft2t9AUBqwo_mgZedLYvkDVOdX8W9wxLYfV0VnCjHl7FLuvuiRs/s1600/geneticistss.jpg" height="198" width="320" /></a></td></tr>
<tr><td class="tr-caption" style="text-align: center;">An informational graphic of the process of gene duplication, showing how sister genes can confer mutational robustness by allowing organisms to adapt to novel environments. Credit: Mario Fares, 2014. </td></tr>
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Source: <a href="http://phys.org/news/2014-09-geneticists-year-old-dilemma-duplicate-genes.html"><span style="color: yellow;"><b>Phys.org</b></span></a></div>
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Geneticists at Trinity College Dublin have made a major breakthrough with important implications for understanding the evolution of genomes in a variety of organisms.<br />
They found a mechanism sought for more than four decades that explains how gene duplication leads to novel functions in individuals.<br />
Gene duplication is a biological phenomenon that leads to the sudden emergence of new genetic material. 'Sister' <a class="textTag" href="http://phys.org/tags/genes/" rel="tag">genes</a> – the products of gene duplication – can survive across long evolutionary timescales, and allow organisms to tolerate otherwise lethal mutations.<br />
The Trinity geneticists have now identified and described the mechanism underlying this increased tolerance, which is known as 'mutational robustness'.<br />
By experimentally demonstrating that this robustness is important for <a class="textTag" href="http://phys.org/tags/yeast+cells/" rel="tag">yeast cells</a> to adapt to novel conditions, including those that are stressful to the cells, they have underlined the likely reason for the existence of gene duplication.<br />
"Natural selection - a process that keeps essential things in the cell - also removes genes that are redundant from the genome," said Dr Mario A Fares, Assistant Professor in Genetics at Trinity, and leading author of the study.<br />
"The mechanism resolving the conflict between sister genes and their apparent evolutionary instability had remained a mystery for decades, but we have now cracked this latest part of the genetic code."<br />
Gene duplication is a frequent phenomenon in <a class="textTag" href="http://phys.org/tags/eukaryotic+organisms/" rel="tag">eukaryotic organisms</a> (which safeguard their <a class="textTag" href="http://phys.org/tags/genetic+material/" rel="tag">genetic material</a> within cell membranes), including yeast, plants, and animals. But understanding how duplication leads to biological innovation is difficult because evolution cannot be easily traced seeing as it occurs on timescales in the order of millions of years.<br />
Despite their apparently redundant nature, duplicate genes that originated 100 million years ago can still be found in today's organisms. This phenomenon has always suggested the existence of a mechanism maintaining them in the genomes. The researchers in this study chose to work with yeast – an organism whose entire genome has been duplicated over time – to join up the dots. <br />
They 'evolved' yeast cells in the laboratory under conditions that allowed the spread of mutations rejected by natural selection, by simply reducing the effect that <a class="textTag" href="http://phys.org/tags/natural+selection/" rel="tag">natural selection</a> had on these 'maladapted' cells. They found that duplicate genes tolerated the maladaptive mutations to a greater degree than non-duplicate genes.<br />
The geneticists' simple experimental approach revealed that these genes, duplicated 100 million years ago, were still able to respond to different environments as they changed, as well as highlighting their potential to generate new adaptations that might give them an advantage in new environments.<br />
"Discovering the mechanism of innovation through <a class="textTag" href="http://phys.org/tags/gene+duplication/" rel="tag">gene duplication</a> marks an exciting beginning for a new era of research in which evolution can be conducted in the laboratory and theories hitherto speculative tested," added Dr Fares.<br />
"Our discovery also has implications for explaining the importance of redundancy in the human society as well. The role of increased redundancies in a fashioned job market in lenient economical conditions could lead, in crisis times, to the emergence of new companies, specialized workforces, and the optimization of individual capabilities, for example, although this requires a profound investigation."<br />
The research, recently published online in the high-profile international journal, <i>Genome Research</i>, was supported by Science Foundation Ireland (SFI).<br />
<section><b>Explore further:</b> <a href="http://medicalxpress.com/news/2014-04-evolution-duplicate-genes.html#inlRlv" itemprop="relatedLink">New study explains evolution of duplicate genes</a><br />
<b>Journal reference:</b> <!--news infobox //--> <a class="textTag" href="http://phys.org/journals/genome-research/" rel="news">Genome Research</a><br />
<b>Provided by</b> <!--news infobox //--> <a class="textTag" href="http://phys.org/partners/trinity-college-dublin/" rel="news">Trinity College Dublin</a> </section>olosciencehttp://www.blogger.com/profile/07007258673266741468noreply@blogger.com0tag:blogger.com,1999:blog-4305283407805626298.post-2846572653152893422010-01-14T12:06:00.001-08:002010-01-14T12:09:05.052-08:00Biologists Wake Dormant Viruses and Uncover Mechanism for Survival.<div align="center"><a href="http://www.sciencedaily.com/images/2010/01/100113131512.jpg"><img style="TEXT-ALIGN: center; MARGIN: 0px auto 10px; WIDTH: 300px; DISPLAY: block; HEIGHT: 211px; CURSOR: hand" border="0" alt="" src="http://www.sciencedaily.com/images/2010/01/100113131512.jpg" /></a> <strong><em><span style="font-size:85%;">This shows the functioning of Kap1 protein in mouse embrocation cells. (Credit: Pascal Coderay, </span></em></strong><a href="mailto:pascal@salut.ch"><strong><em><span style="font-size:85%;">pascal@salut.ch</span></em></strong></a><strong><em><span style="font-size:85%;">)</span></em> </strong></div><div align="center"><strong>Source: </strong><a href="http://www.sciencedaily.com/releases/2010/01/100113131512.htm"><strong><span style="color:#ffff66;">ScienceDaily<br /></span></strong></div></a><div align="center"><strong>---------------------------</strong></div><div align="left"><strong>ScienceDaily (Jan. 14, 2010) — It is known that viral "squatters" comprise nearly half of our genetic code. These genomic invaders inserted their DNA into our own millions of years ago when they infected our ancestors. But just how we keep them quiet and prevent them from attack was more of a mystery until EPFL researchers revived them. </strong></div><div align="left"><strong>The reason we survive the presence of these endogenous retroviruses -- viruses that attack and are passed on through germ cells, the cells that give rise to eggs and sperm -- is because something keeps the killers silent. Now, publishing in the journal Nature, Didier Trono and his team from EPFL, in Switzerland, describe the mechanism. Their results provide insights into evolution and suggest potential new therapies in fighting another retrovirus -- HIV.<br />By analysing embryonic stem cells in mice within the first few days of life, Trono and team discovered that mouse DNA codes for an army of auxiliary proteins that recognize the numerous viral sequences littering the genome. The researchers also demonstrated that a master regulatory protein called KAP1 appears to orchestrate these inhibitory proteins in silencing would-be viruses. When KAP1 is removed, for example, the viral DNA "wakes up," multiplies, induces innumerable mutations, and the embryo soon dies.<br />Because retroviruses tend to mutate their host's DNA, they have an immense power and potential to alter genes. And during ancient pandemics, some individuals managed to silence the retrovirus involved and therefore survived to pass on the ability. Trono explains that the great waves of endogenous retrovirus appearance coincide with times when evolution seemed to leap ahead.<br />"In our genome we find traces of the last two major waves. The first took place 100 million years ago, at the time when mammals started to develop, and the second about fifty million years ago, just before the first anthropoid primates," he says.<br />The discovery of the KAP1 mechanism could be of interest in the search for new therapeutic approaches to combat AIDS. The virus that causes AIDS can lie dormant in the red blood cells it infects, keeping it hidden from potential treatments. Waking the virus up could expose it to attack.<br />Co-authors include Helen M. Rowe, School of Life Sciences, École Polytechnique Fédérale de Lausanne (EPFL), Switzerland; Johan Jakobsson, EPFL and Wallenberg Neuroscience Center, Department of Experimental Medical Sciences, Lund University, Sweden; Daniel Mesnard, EPFL; Jacques Rougemont, EPFL; Séverine Reynard, EPFL; Tugce Aktas, EMBL Heidelberg, Germany; Pierre V. Maillard, EPFL; Hillary Layard-Liesching, EPFL; Sonia Verp, EPFL; Julien Marquis, EPFL; François Spitz, EMBL Heidelberg, Germany; Daniel B. Constam, EPFL; and Didier Trono, EPFL. </strong></div><div align="left"><strong>Story Source:<br />Adapted from materials provided by </strong><a class="blue" href="http://www.epfl.ch/" rel="nofollow" target="_blank"><strong>Ecole Polytechnique Fédérale de Lausanne</strong></a><strong>, via </strong><a href="http://www.eurekalert.org/" rel="nofollow" target="_blank"><strong>EurekAlert!</strong></a><strong>, a service of AAAS. </strong></div>olosciencehttp://www.blogger.com/profile/07007258673266741468noreply@blogger.com1tag:blogger.com,1999:blog-4305283407805626298.post-78880187332037262842010-01-14T07:17:00.000-08:002010-01-14T07:19:50.372-08:00Chimp and human Y chromosomes evolving faster than expected.<div align="center"><a href="http://cdn.physorg.com/newman/gfx/news/chimpandhuma.jpg"><img style="TEXT-ALIGN: center; MARGIN: 0px auto 10px; WIDTH: 260px; DISPLAY: block; HEIGHT: 254px; CURSOR: hand" border="0" alt="" src="http://cdn.physorg.com/newman/gfx/news/chimpandhuma.jpg" /></a><strong> Source: </strong><a href="http://www.physorg.com/news182605704.html"><strong><span style="color:#ffff66;">Physorg.com</span></strong></a></div><div align="center"><strong>-------------------------</strong></div><div align="left"><strong>Contrary to a widely held scientific theory that the mammalian Y chromosome is slowly decaying or stagnating, new evidence suggests that in fact the Y is actually evolving quite rapidly through continuous, wholesale renovation. </strong></div><div align="left"><strong>By conducting the first comprehensive interspecies comparison of Y chromosomes, Whitehead Institute researchers have found considerable differences in the genetic sequences of the human and chimpanzee Ys—an indication that these chromosomes have evolved more quickly than the rest of their respective genomes over the 6 million years since they emerged from a </strong><a class="textTag" href="http://www.physorg.com/tags/common+ancestor/" rel="tag"><strong>common ancestor</strong></a><strong>. The findings are published online this week in the journal Nature.<br />"The region of the Y that is evolving the fastest is the part that plays a role in sperm production," say Jennifer Hughes, first author on the Nature paper and a postdoctoral researcher in Whitehead Institute Director David Page's lab. "The rest of the Y is evolving more like the rest of the </strong><a class="textTag" href="http://www.physorg.com/tags/genome/" rel="tag"><strong>genome</strong></a><strong>, only a little bit faster."<br />The chimp </strong><a class="textTag" href="http://www.physorg.com/tags/y+chromosome/" rel="tag"><strong>Y chromosome</strong></a><strong> is only the second Y chromosome to be comprehensively sequenced. The original chimp genome sequencing completed in 2005 largely excluded the Y chromosome because its hundreds of repetitive sections typically confound standard sequencing techniques. Working closely with the Genome Center at Washington University, the Page lab managed to painstakingly sequence the chimp Y chromosome, allowing for comparison with the human Y, which the Page lab and the Genome Center at Washington University had sequenced successfully back in 2003.<br />The results overturned the expectation that the chimp and human Y chromosomes would be highly similar. Instead, they differ remarkably in their structure and gene content. The chimp Y, for example, has lost one third to one half of the human Y chromosome genes--a significant change in a relatively short period of time. Page points out that this is not all about gene decay or loss. He likens the Y chromosome changes to a home undergoing continual renovation.<br />"People are living in the house, but there's always some room that's being demolished and reconstructed," says Page, who is also a Howard Hughes Medical Institute investigator. "And this is not the norm for the genome as a whole."<br /><br />Wes Warren, Assistant Director of the Washington University Genome Center, agrees. "This work clearly shows that the Y is pretty ingenious at using different tools than the rest of the genome to maintain diversity of genes," he says. "These findings demonstrate that our knowledge of the Y chromosome is still advancing."<br />Hughes and Page theorize that the divergent evolution of the </strong><a class="textTag" href="http://www.physorg.com/tags/chimp/" rel="tag"><strong>chimp</strong></a><strong> and human Y chromosomes may be due to several factors, including traits specific to Y chromosomes and differences in mating behaviors.<br />Because multiple male </strong><a class="textTag" href="http://www.physorg.com/tags/chimpanzees/" rel="tag"><strong>chimpanzees</strong></a><strong> may mate with a single female in rapid succession, the males' sperm wind up in heated reproductive competition. If a given male produces more sperm, that male would theoretically be more likely to impregnate the female, thereby passing on his superior sperm production genes, some of which may be residing on the Y chromosome, to the next generation.<br />Because selective pressure to pass on advantageous sperm production genes is so high, those genes may also drag along detrimental genetic traits to the next generation. Such transmission is allowed to occur because, unlike other chromosomes, the Y has no partner with which to swap genes during cell division. Swapping genes between chromosomal partners can eventually associate positive gene versions with each other and eliminate detrimental gene versions. Without this ability, the Y chromosome is treated by evolution as one large entity. Either the entire chromosome is advantageous, or it is not.<br />In chimps, this potent combination of intense selective pressure on sperm production genes and the inability to swap genes may have fueled the Y chromosome's rapid evolution. Disadvantages from a less-than-ideal gene version or even the deletion of a section of the chromosome may have been outweighed by the advantage of improved </strong><a class="textTag" href="http://www.physorg.com/tags/sperm/" rel="tag"><strong>sperm</strong></a><strong> production, resulting in a Y chromosome with far fewer </strong><a class="textTag" href="http://www.physorg.com/tags/genes/" rel="tag"><strong>genes</strong></a><strong> than its human counterpart.<br />To determine whether this rapid rate of evolution affects Y chromosomes beyond those of chimps and humans, the Page lab and the Washington University Genome Center are now sequencing and examining the Y chromosomes of several other mammals.<br />Provided by Massachusetts Institute of Technology.</strong></div>olosciencehttp://www.blogger.com/profile/07007258673266741468noreply@blogger.com0tag:blogger.com,1999:blog-4305283407805626298.post-526965948450982322010-01-13T12:11:00.001-08:002010-01-13T12:14:18.256-08:00Scientists sequence soybean genome, reveal pathways for improving biodiesel.<div align="center"><a href="http://cdn.physorg.com/newman/gfx/news/soybeangenom.jpg"><img style="TEXT-ALIGN: center; MARGIN: 0px auto 10px; WIDTH: 260px; DISPLAY: block; HEIGHT: 282px; CURSOR: hand" border="0" alt="" src="http://cdn.physorg.com/newman/gfx/news/soybeangenom.jpg" /></a> <strong><em><span style="font-size:85%;">Soybean, one of the most important global sources of protein and oil, is now the first legume species with a published complete draft genome sequence. Credit: Roy Kaltschmidt, Lawrence Berkeley National Laboratory.</span></em></strong></div><div align="center"><strong>-------------------------</strong></div><div align="center"><strong>Source: </strong><a href="http://www.physorg.com/news182606405.html"><strong><span style="color:#ffff66;">Physorg.com</span></strong></a></div><div align="center"><strong>-------------------------</strong></div><div align="left"><strong>Soybean, one of the most important global sources of protein and oil, is now the first legume species with a published complete draft genome sequence. The sequence and its analysis appear in the January 14 edition of the journal Nature. </strong></div><div align="left"><br /><strong>The research team comprised 18 institutions, including the U.S. Department of Energy Joint Genome Institute (DOE JGI), the U.S. Department of Agriculture-Agricultural Research Service (USDA-ARS), Purdue University and the University of North Carolina at Charlotte. The DOE, National Science Foundation, USDA and United </strong><a class="textTag" href="http://www.physorg.com/tags/soybean/" rel="tag"><strong>Soybean</strong></a><strong> Board supported the research.<br />"The soybean genome's billion-plus nucleotides afford us a better understanding of the plant's capacity to turn sunlight, carbon dioxide, nitrogen and water, into concentrated energy, </strong><a class="textTag" href="http://www.physorg.com/tags/protein/" rel="tag"><strong>protein</strong></a><strong>, and nutrients for human and animal use," said Anna Palmisano, DOE Associate Director of Science for Biological and Environmental Research. "This opens the door to crop improvements that are sorely needed for energy production, sustainable human and animal food production, and a healthy environmental balance in agriculture worldwide."<br />With the soybean genetic code now determined, the research community has access to a key reference for more than 20,000 legume species and can explore the extraordinary evolutionary innovation of nitrogen-fixing symbiosis that is so critically important to successful agricultural </strong><a class="textTag" href="http://www.physorg.com/tags/crop+rotation/" rel="tag"><strong>crop rotation</strong></a><strong> strategies.<br />Jeremy Schmutz, the study's first author and a DOE JGI scientist at the HudsonAlpha Institute for Biotechnology in Alabama, said that the soybean sequencing was the largest plant project done to date at the DOE Joint Genome Institute. "It also happens to be the largest plant that's ever been sequenced by the whole genome shotgun strategy—where we break it apart and reassemble it like a huge puzzle," he said. Of the more than 20 other plant genomes taken on by the DOE JGI, those already sequenced include the black cottonwood (poplar) tree and the grain sorghum, both targeted because of their promise as biomass feedstocks for biofuels production.<br />"This is a milestone for soybean research and promises to usher in a new era in soybean agronomic improvement," said co-author Gary Stacey, Director, Center for Sustainable Energy and Associate Director and National Center for Soybean Biotechnology, University of Missouri. "The genome provides a parts list of what it takes to make a soybean plant and, more importantly, helps to identify those genes that are essential for such important agronomic traits as protein and oil content." </strong></div><div align="left"><strong></strong> </div><div align="left"><strong>From the sequence analysis, Stacey said that he and his colleagues have identified more than 46,000 genes of which 1,110 are involved in lipid metabolism. "These genes and their associated pathways are the building blocks for soybean oil content and represent targets that can be modified to bolster output and lead to the increase of the use of soybean oil for biodiesel production."<br />While </strong><a class="textTag" href="http://www.physorg.com/tags/biodiesel/" rel="tag"><strong>biodiesel</strong></a><strong> from soybean oil represents a cleaner, renewable alternative to fossil fuels with desirable properties as a liquid transportation fuel, there simply is not enough oil produced by the plant to be a competitive gasoline on a gallons-of-fuel yield per acre. The availability of the </strong><a class="textTag" href="http://www.physorg.com/tags/soybean+genome/" rel="tag"><strong>soybean genome</strong></a><strong> may provide some key solutions. "We can now zero in on the control points governing carbon flow towards protein and oil," said Tom Clemente, Professor, Center for Biotechnology, Center for Plant Science Innovation at the University of Nebraska, Lincoln. "With the combination of informatics, biochemistry and genetics we can target the development of a soybean with greater than 40 percent oil content."<br />The availability of the soybean genome sequence has accelerated other soybean trait discovery efforts as well. For example, researchers have used the sequence to zero in on a mutation that can be used to select for a line that has lower levels of the sugar stachyose, which will improve the ability of animals and humans to digest soybeans.</strong></div><div align="left"><strong></strong> </div><div align="left"><strong>In another effort, by comparing the genomes of soybean and corn, a single-base pair mutation was found that causes a reduction in phytate production in soybean. Phytate is the form in which phosphorous is stored in plant tissue. Because phytate is not absorbed by the animals that eat the feed, the unabsorbed phytate passes through the gastrointestinal tract, elevating the amount of phosphorus in the manure. Limiting phytate production in the soybean could reduce a major environmental runoff contaminant from swine and poultry waste.<br />Of additional importance for soybean farmers is that the genome sequence has provided access to the first resistance gene for the devastating disease Asian Soybean Rust (ASR). In countries where ASR is well established, soybean yield losses due to the disease can be as high as 80 percent.</strong></div><div align="left"><br /><strong>Provided by DOE/Joint Genome Institute </strong></div>olosciencehttp://www.blogger.com/profile/07007258673266741468noreply@blogger.com1tag:blogger.com,1999:blog-4305283407805626298.post-3848969163040737262010-01-13T11:55:00.001-08:002010-01-13T11:58:10.940-08:00Chimp and Human Y Chromosomes Evolving Faster Than Expected.<div align="center"><a href="http://www.sciencedaily.com/images/2010/01/100113131505.jpg"><img style="TEXT-ALIGN: center; MARGIN: 0px auto 10px; WIDTH: 300px; DISPLAY: block; HEIGHT: 199px; CURSOR: hand" border="0" alt="" src="http://www.sciencedaily.com/images/2010/01/100113131505.jpg" /></a> <strong><em><span style="font-size:85%;">Contrary to a widely held scientific theory that the mammalian Y chromosome is slowly decaying or stagnating, new evidence suggests that in fact the Y is actually evolving quite rapidly through continuous, wholesale renovation. (Credit: iStockphoto/Wesley Jenkins) </span></em></strong></div><div align="center"><strong><em><span style="font-size:85%;"></span></em></strong> </div><div align="center"><strong>Source: </strong><a href="http://www.sciencedaily.com/releases/2010/01/100113131505.htm"><strong><span style="color:#ffff66;">ScienceDaily</span></strong></a></div><div align="center"><strong>-------------------------</strong></div><div align="left"><strong>ScienceDaily (Jan. 13, 2010) — Contrary to a widely held scientific theory that the mammalian Y chromosome is slowly decaying or stagnating, new evidence suggests that in fact the Y is actually evolving quite rapidly through continuous, wholesale renovation. </strong></div><div align="left"><strong>By conducting the first comprehensive interspecies comparison of Y chromosomes, Whitehead Institute researchers have found considerable differences in the genetic sequences of the human and chimpanzee Ys -- an indication that these chromosomes have evolved more quickly than the rest of their respective genomes over the 6 million years since they emerged from a common ancestor. The findings are published online this week in the journal Nature.<br />"The region of the Y that is evolving the fastest is the part that plays a role in sperm production," say Jennifer Hughes, first author on the Nature paper and a postdoctoral researcher in Whitehead Institute Director David Page's lab. "The rest of the Y is evolving more like the rest of the genome, only a little bit faster."<br />The chimp Y chromosome is only the second Y chromosome to be comprehensively sequenced. The original chimp genome sequencing completed in 2005 largely excluded the Y chromosome because its hundreds of repetitive sections typically confound standard sequencing techniques. Working closely with the Genome Center at Washington University, the Page lab managed to painstakingly sequence the chimp Y chromosome, allowing for comparison with the human Y, which the Page lab and the Genome Center at Washington University had sequenced successfully back in 2003.<br />The results overturned the expectation that the chimp and human Y chromosomes would be highly similar. Instead, they differ remarkably in their structure and gene content. The chimp Y, for example, has lost one third to one half of the human Y chromosome genes--a significant change in a relatively short period of time. Page points out that this is not all about gene decay or loss. He likens the Y chromosome changes to a home undergoing continual renovation.<br />"People are living in the house, but there's always some room that's being demolished and reconstructed," says Page, who is also a Howard Hughes Medical Institute investigator. "And this is not the norm for the genome as a whole."<br />Wes Warren, Assistant Director of the Washington University Genome Center, agrees. "This work clearly shows that the Y is pretty ingenious at using different tools than the rest of the genome to maintain diversity of genes," he says. "These findings demonstrate that our knowledge of the Y chromosome is still advancing."<br />Hughes and Page theorize that the divergent evolution of the chimp and human Y chromosomes may be due to several factors, including traits specific to Y chromosomes and differences in mating behaviors.<br />Because multiple male chimpanzees may mate with a single female in rapid succession, the males' sperm wind up in heated reproductive competition. If a given male produces more sperm, that male would theoretically be more likely to impregnate the female, thereby passing on his superior sperm production genes, some of which may be residing on the Y chromosome, to the next generation.<br />Because selective pressure to pass on advantageous sperm production genes is so high, those genes may also drag along detrimental genetic traits to the next generation. Such transmission is allowed to occur because, unlike other chromosomes, the Y has no partner with which to swap genes during cell division. Swapping genes between chromosomal partners can eventually associate positive gene versions with each other and eliminate detrimental gene versions. Without this ability, the Y chromosome is treated by evolution as one large entity. Either the entire chromosome is advantageous, or it is not.<br />In chimps, this potent combination of intense selective pressure on sperm production genes and the inability to swap genes may have fueled the Y chromosome's rapid evolution. Disadvantages from a less-than-ideal gene version or even the deletion of a section of the chromosome may have been outweighed by the advantage of improved sperm production, resulting in a Y chromosome with far fewer genes than its human counterpart.<br />To determine whether this rapid rate of evolution affects Y chromosomes beyond those of chimps and humans, the Page lab and the Washington University Genome Center are now sequencing and examining the Y chromosomes of several other mammals.<br />This research was funded by the National Institutes of Health (NIH) and the Howard Hughes Medical Institute (HHMI). </strong></div><div align="left"><strong>Story Source:<br />Adapted from materials provided by </strong><a class="blue" href="http://www.wi.mit.edu/index.html" rel="nofollow" target="_blank"><strong>Whitehead Institute for Biomedical Research</strong></a><strong>. Original article written by Nicole Giese.<br />Journal Reference:<br />1. Jennifer F. Hughes, Helen Skaletsky, Tatyana Pyntikova, Tina A. Graves, Saskia K. M. Van Daalen, Patrick J. Minx, Robert S. Fulton, Sean D. Mcgrath, Devin P. Locke, Cynthia Friedman, Barbara J. Trask, Elaine R. Mardis, Wesley C. Warren, Sjoerd Repping, Steve Rozen, Richard K. Wilson, David C. Page. Chimpanzee and human Y chromosomes are remarkably divergent in structure and gene content. Nature, Online January 13, 2010 </strong></div>olosciencehttp://www.blogger.com/profile/07007258673266741468noreply@blogger.com0tag:blogger.com,1999:blog-4305283407805626298.post-26035069342918561112010-01-13T01:16:00.000-08:002010-01-13T01:19:26.979-08:00'Longevity Gene' Helps Prevent Memory Decline and Dementia.<div align="center"><a href="http://www.sciencedaily.com/images/2010/01/100112165234.jpg"><img style="TEXT-ALIGN: center; MARGIN: 0px auto 10px; WIDTH: 300px; DISPLAY: block; HEIGHT: 199px; CURSOR: hand" border="0" alt="" src="http://www.sciencedaily.com/images/2010/01/100112165234.jpg" /></a> <strong><em><span style="font-size:85%;">Scientists at Albert Einstein College of Medicine of Yeshiva University have found that a "longevity gene" helps to slow age-related decline in brain function in older adults. Drugs that mimic the gene's effect are now under development, the researchers note, and could help protect against Alzheimer's disease. (Credit: iStockphoto/Anne De Haas) </span></em></strong></div><strong></strong><br /><div align="center"><strong>Source: </strong><a href="http://www.sciencedaily.com/releases/2010/01/100112165234.htm"><strong><span style="color:#ffff66;">ScienceDaily</span></strong></a></div><div align="center"><strong>--------------------------</strong></div><div align="left"><strong>ScienceDaily (Jan. 13, 2010) — Scientists at Albert Einstein College of Medicine of Yeshiva University have found that a "longevity gene" helps to slow age-related decline in brain function in older adults. Drugs that mimic the gene's effect are now under development, the researchers note, and could help protect against Alzheimer's disease. </strong></div><div align="left"><strong>The paper describing the Einstein study is published in the January 13 edition of the Journal of the American Medical Association.<br />"Most work on the genetics of Alzheimer's disease has focused on factors that increase the danger," said Richard B. Lipton, M.D., the Lotti and Bernard Benson Faculty Scholar in Alzheimer's Disease and professor and vice chair in the Saul R. Korey Department of Neurology at Einstein and senior author of the paper. As an example, he cites APOE ε4, a gene variant involved in cholesterol metabolism that is known to increase the risk of Alzheimer's among those who carry it.<br />"We reversed this approach," says Dr. Lipton, "and instead focused on a genetic factor that protects against age-related illnesses, including both memory decline and Alzheimer's disease."<br />In a 2003 study, Dr. Lipton and his colleagues identified the cholesteryl ester transfer protein (CETP) gene variant as a "longevity gene" in a population of Ashkenazi Jews. The favorable CETP gene variant increases blood levels of high-density lipoprotein (HDL) -- the so-called good cholesterol -- and also results in larger-than-average HDL and low-density lipoprotein (LDL) particles.<br />The researchers of the current study hypothesized that the CETP longevity gene might also be associated with less cognitive decline as people grow older. To find out, they examined data from 523 participants from the Einstein Aging Study, an ongoing federally funded project that has followed a racially and ethnically diverse population of elderly Bronx residents for 25 years.<br />At the beginning of the study, the 523 participants -- all of them 70 or over -- were cognitively healthy, and their blood samples were analyzed to determine which CETP gene variant they carried. They were then followed for an average of four years and tested annually to assess their rates of cognitive decline, the incidence of Alzheimer's disease and other changes.<br />"We found that people with two copies of the longevity variant of CETP had slower memory decline and a lower risk for developing dementia and Alzheimer's disease," says Amy E. Sanders, M.D., assistant professor in the Saul R. Korey Department of Neurology at Einstein and lead author of the paper. "More specifically, those participants who carried two copies of the favorable CETP variant had a 70 percent reduction in their risk for developing Alzheimer's disease compared with participants who carried no copies of this gene variant."<br />The favorable gene variant alters CETP so that the protein functions less well than usual. Dr. Lipton notes that drugs are now being developed that duplicate this effect on the CETP protein. "These agents should be tested for their ability to promote successful aging and prevent Alzheimer's disease," he recommends.<br />The research was funded by the National Institute on Aging, one of the 27 institutes and centers of the National Institutes of Health. </strong></div><div align="left"><strong>Story Source:<br />Adapted from materials provided by </strong><a class="blue" href="http://www.aecom.yu.edu/" rel="nofollow" target="_blank"><strong>Albert Einstein College of Medicine</strong></a><strong>. </strong></div><div align="left"><strong>Journal Reference:<br />1. Sanders et al. Association of a Functional Polymorphism in the Cholesteryl Ester Transfer Protein (CETP) Gene With Memory Decline and Incidence of Dementia. JAMA The Journal of the American Medical Association, 2010; 303 (2): 150 DOI: </strong><a href="http://dx.doi.org/10.1001/jama.2009.1988" rel="nofollow" target="_blank"><strong>10.1001/jama.2009.1988</strong></a><strong> </strong></div>olosciencehttp://www.blogger.com/profile/07007258673266741468noreply@blogger.com0tag:blogger.com,1999:blog-4305283407805626298.post-9638627921005849262010-01-12T07:48:00.000-08:002010-01-12T07:51:56.715-08:00Scientists discover new protein function.<div align="center"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhGq-vhrrscL-O4LgxLA3Z4TjlL5XltkoqIeWsqKrVgNWmZRvvw5DBehpMq1hyNlHZsIayQSJAaJKNNYUOuKHSEOLtl05KiBxp9u80hZjp4uG7oqWk9iGz96EsD_YG4I5girrDKXC-h-PM/s1600-h/protein.jpg"><img style="TEXT-ALIGN: center; MARGIN: 0px auto 10px; WIDTH: 320px; DISPLAY: block; HEIGHT: 240px; CURSOR: hand" id="BLOGGER_PHOTO_ID_5425881262289757378" border="0" alt="" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEhGq-vhrrscL-O4LgxLA3Z4TjlL5XltkoqIeWsqKrVgNWmZRvvw5DBehpMq1hyNlHZsIayQSJAaJKNNYUOuKHSEOLtl05KiBxp9u80hZjp4uG7oqWk9iGz96EsD_YG4I5girrDKXC-h-PM/s320/protein.jpg" /></a><strong> Source: <a href="http://www.physorg.com/news182515286.html"><span style="color:#ffff66;">Physorg.com </span></a></strong></div><div align="center"><strong>------------------------</strong></div><div align="left"><strong>Carnegie Mellon University's Philip R. LeDuc and his collaborators in Massachusetts and Taiwan have discovered a new function of a protein that could ultimately unlock the mystery of how these workhorses of the body play a central role in the mechanics of biological processes in people. </strong></div><div align="left"><br /><strong>"What we have done is find a new function of a </strong><a class="textTag" href="http://www.physorg.com/tags/protein/" rel="tag"><strong>protein</strong></a><strong> that helps control cell behavior from a mechanics perspective," said LeDuc, an associate professor of mechanical engineering with courtesy appointments in the Biomedical Engineering, Biological Sciences and Computational Biology departments.<br />"For over 15 years, researchers have been mainly focusing on a protein called Integrin to study these cell functions, but our team found that another lesser known protein called Syndecan-4 is extremely important in cell behavior in a field called MechanoBiology (a field linking mechanics and biology). Syndecan-4 is known to play an essential role in a variety of diseases like cancer," LeDuc said.<br />LeDuc's new findings appear in the Dec. 29 edition of the prestigious journal </strong><a class="textTag" href="http://www.physorg.com/tags/proceedings+of+the+national+academy+of+sciences/" rel="tag"><strong>Proceedings of the National Academy of Sciences</strong></a><strong> along with complementary work that is appearing in another highly respected journal, Nature Protocols.<br />Essentially what his research does is take a look at how a protein's shape and form determines how it functions in the human body from a mechanics perspective. Proteins are composed of long chains of </strong><a class="textTag" href="http://www.physorg.com/tags/amino+acids/" rel="tag"><strong>amino acids</strong></a><strong> than can form bonds with other molecules in a chain, kinking, twisting and folding into complicated, three-dimensional shapes, such as helices or densely furrowed globular structures.<br />"These folded shapes are immensely important because they can define a protein's function in the cell," said LeDuc, who is also developing novel biologically inspired diagnostic approaches and materials as well as computational methods to understand molecular behavior.<br />LeDuc said his research finds that some protein shapes fit perfectly into cell receptors, turning chemical processes on and off, like a key in a lock. With mechanics changing the shape of proteins, LeDuc says the key might no longer fit into the lock, and serious consequences in the body can occur when proteins fail to assume their preordained shapes or fail to connect properly.<br />"Misguided proteins have been linked to disease such as cancer, arthritis and wound healing, among others," LeDuc said. "Our research is looking at how protein shapes affect </strong><a class="textTag" href="http://www.physorg.com/tags/cells/" rel="tag"><strong>cells</strong></a><strong> and how cell biomechanics impacts the entire process."<br />Provided by Carnegie Mellon University</strong></div>olosciencehttp://www.blogger.com/profile/07007258673266741468noreply@blogger.com0tag:blogger.com,1999:blog-4305283407805626298.post-36321872474240963962010-01-12T00:16:00.001-08:002010-01-12T00:18:17.864-08:00Genome of Woodland Strawberry, a Model System for Rosaceae Plants, Sequenced.<div align="center"><a href="http://www.sciencedaily.com/images/2010/01/100111172010.jpg"><img style="TEXT-ALIGN: center; MARGIN: 0px auto 10px; WIDTH: 300px; DISPLAY: block; HEIGHT: 211px; CURSOR: hand" border="0" alt="" src="http://www.sciencedaily.com/images/2010/01/100111172010.jpg" /></a> <strong>Source: </strong><a href="http://www.sciencedaily.com/releases/2010/01/100111172010.htm"><strong><span style="color:#ffff66;">ScienceDaily</span></strong></a></div><div align="center"><strong>--------------------------</strong></div><div align="left"><strong>ScienceDaily (Jan. 12, 2010) — The genome of a model plant related to peach, cherry and cultivated strawberry has been sequenced by a consortium of international researchers that includes scientists with the Agricultural Research Service (ARS). </strong></div><div align="left"><strong>Fragaria vesca, commonly known as the woodland or alpine strawberry, is a member of the Rosaceae family, which consists of more than 100 genera and 3,000 species. This large family includes many economically important and popular fruit, nut, ornamental and woody crops, such as almond, apple, peach, cherry, raspberry, strawberry and rose.<br />F. vesca has many traits that make it an attractive model system for functional genomics studies. Its small size and rapid life cycle enable researchers to conduct genetic analyses with great efficiency and low cost. To determine the importance of a gene of interest, F. vesca can be transformed in order to modulate the activity of that gene in the plant. Most importantly, F. vesca has a relatively small genome, yet shares most gene sequences with other members of the Rosaceae family, making it an important tool for addressing questions regarding gene function.<br />ARS molecular biologist Janet Slovin, with the Genetic Improvement of Fruits and Vegetables Laboratory in Beltsville, Md., created the nearly inbred line used in the F. vesca genome sequencing project. Named "Hawaii 4," this line allowed the researchers to more easily program a computer to piece the genome together from the relatively short lengths of sequence data generated by modern sequencing machines.<br />Although the F. vesca genome is a model genome for the Rosaceae group, critical regulatory gene functions will probably differ, hypothesizes Slovin. Scientists can use the genome sequence to identify these genes, to test their function in F. vesca, and to develop molecular genetic markers for more rapid breeding of crops belonging to the Rosaceae group. Slovin will use the genome to study and improve heat tolerance during fruit production in strawberry.<br />The scientists announced the sequencing of the genome of woodland strawberry January 9 at the Plant and Animal Genome Conference in San Diego, Ca. The project was funded by Roche Diagnostics. </strong></div><div align="left"><strong>Story Source:<br />Adapted from materials provided by </strong><a class="blue" href="http://www.csrees.usda.gov/" rel="nofollow" target="_blank"><strong>United States Department of Agriculture-Research, Education, and Economics</strong></a><strong>. </strong></div>olosciencehttp://www.blogger.com/profile/07007258673266741468noreply@blogger.com0tag:blogger.com,1999:blog-4305283407805626298.post-16636486482253458502010-01-11T13:32:00.001-08:002010-01-11T13:32:52.440-08:00Statistics Page<p align="center"><a title="free world map tracker" href="http://24counter.com/vmap/1258031813/"><img title="free world map counter" border="1" alt="world map hits counter" src="http://24counter.com/map/view.php?type=180&id=1258031813" /></a></p><div align="center"><br /><a href="http://24counter.com/map/">map counter</a><br /><br /><a href="http://24counter.com/cc_stats/1258031831/" target="_blank"><img border="0" alt="blog counter" src="http://24counter.com/online/ccc.php?id=1258031831" /></a><br /><br /><a href="http://24counter.com/">blog counter</a><br /><br /><a href="http://24counter.com/conline/1258031831/" target="_blank"><img border="0" alt="visitors by country counter" src="http://24counter.com/online/fcc.php?id=1258031831" /></a><br /><a href="http://24counter.com/" target="_blank">flag counter</a></div>olosciencehttp://www.blogger.com/profile/07007258673266741468noreply@blogger.com0tag:blogger.com,1999:blog-4305283407805626298.post-76191870368896456402010-01-10T01:29:00.000-08:002010-01-10T01:32:30.111-08:00Evolutionary Surprise: Eight Percent of Human Genetic Material Comes from a Virus.<div align="center"><a href="http://www.sciencedaily.com/images/2010/01/100107103621.jpg"><img style="TEXT-ALIGN: center; MARGIN: 0px auto 10px; WIDTH: 300px; DISPLAY: block; HEIGHT: 225px; CURSOR: hand" border="0" alt="" src="http://www.sciencedaily.com/images/2010/01/100107103621.jpg" /></a><strong> Source: </strong><a href="http://www.sciencedaily.com/releases/2010/01/100107103621.htm"><strong><span style="color:#ffff66;">ScienceDaily</span></strong></a></div><div align="center"><strong>----------------------------</strong></div><div align="left"><strong>ScienceDaily (Jan. 8, 2010) — About eight percent of human genetic material comes from a virus and not from our ancestors, according to researchers in Japan and the U.S. </strong></div><div align="left"><strong>The study, and an accompanying News & Views article by University of Texas at Arlington biology professor Cédric Feschotte, is published in the journal Nature.<br />The research showed that the genomes of humans and other mammals contain DNA derived from the insertion of bornaviruses, RNA viruses whose replication and transcription takes place in the nucleus. Feschotte wrote on recent research led by Professor Keizo Tomonaga at Osaka University in Japan. Feschotte said this virally transmitted DNA may be a cause of mutation and psychiatric disorders such as schizophrenia and mood disorders.<br />In his article, Feschotte speculates about the role of such viral insertions in causing mutations with evolutionary and medical consequences.<br />The assimilation of viral sequences into the host genome is a process referred to as endogenization. This occurs when viral DNA integrates into a chromosome of reproductive cells and is subsequently passed from parent to offspring. Until now, retroviruses were the only viruses known to generate such endogenous copies in vertebrates. But Feschotte said that scientists have found that non-retroviral viruses called bornaviruses have been endogenized repeatedly in mammals throughout evolution.<br />Bornavirus (BDV) owes its name to the town of Borna, Germany, where a virus epidemic in 1885 wiped out a regiment of cavalry horses. BDV infects a range of birds and mammals, including humans. It is unique because it infects only neurons, establishing a persistent infection in its host's brain, and its entire life cycle takes place in the nucleus of the infected cells. Feschotte said this intimate association of BDV with the cell nucleus prompted researchers to investigate whether bornaviruses may have left behind a record of past infection in the form of endogenous elements. They searched the 234 known eukaryotic genomes (those genomes that have been fully sequenced) for sequences that are similar to that of BDV. "The researchers unearthed a plethora of endogenous Borna-like N (EBLN) elements in many diverse mammals, " Feschotte said.<br />The scientists also were able to recover spontaneous BDV insertions in the chromosomes of human cultured cells persistently infected by BVD.Based on these data, Feschotte proposes that BDV insertions could be a source of mutations in the brain cells of infected individuals.<br />"These data yield a testable hypothesis for the alleged, but still controversial, causative association of BDV infection with schizophrenia and mood disorders," Feschotte said. The research in Feschotte 's laboratory, which largely focuses on transposable elements, the genetic elements that are able to move and replicate within the genomes of virtually all living organisms, is representative of the research under way at UT Arlington, an institution of 28,000 students on its way to becoming a nationally recognized, top-tier research university.</strong></div><div align="left"><strong>Story Source:<br />Adapted from materials provided by </strong><a class="blue" href="http://www.uta.edu/" rel="nofollow" target="_blank"><strong>University of Texas at Arlington</strong></a><strong>. </strong></div><div align="left"><strong>Journal References:<br />1.Masayuki Horie, Tomoyuki Honda, Yoshiyuki Suzuki, Yuki Kobayashi, Takuji Daito, Tatsuo Oshida, Kazuyoshi Ikuta, Patric Jern, Takashi Gojobori, John M. Coffin & Keizo Tomonaga. Endogenous non-retroviral RNA virus elements in mammalian genomes. Nature, 2010; 463 (7277): 84 DOI: </strong><a href="http://dx.doi.org/10.1038/nature08695" rel="nofollow" target="_blank"><strong>10.1038/nature08695</strong></a><br /><strong>2.Cédric Feschotte. Virology: Bornavirus enters the genome. Nature, 2010; 463 (7277): 39 DOI: </strong><a href="http://dx.doi.org/10.1038/463039a" rel="nofollow" target="_blank"><strong>10.1038/463039a</strong></a><strong> </strong></div>olosciencehttp://www.blogger.com/profile/07007258673266741468noreply@blogger.com0tag:blogger.com,1999:blog-4305283407805626298.post-83975090699921170952010-01-10T01:23:00.000-08:002010-01-10T01:25:55.520-08:00Evolution's Footprints in Human Genome Precisely Tracked Using New Approach.<div align="center"><a href="http://www.sciencedaily.com/images/2010/01/100107143905.jpg"><img style="TEXT-ALIGN: center; MARGIN: 0px auto 10px; WIDTH: 300px; DISPLAY: block; HEIGHT: 199px; CURSOR: hand" border="0" alt="" src="http://www.sciencedaily.com/images/2010/01/100107143905.jpg" /></a><strong> Source: </strong><a href="http://www.sciencedaily.com/releases/2010/01/100107143905.htm"><strong><span style="color:#ffff66;">ScienceDaily</span></strong></a></div><div align="center"><strong>---------------------------</strong></div><div align="left"><strong>ScienceDaily (Jan. 8, 2010) — Fossils may provide tantalizing clues to human history but they also lack some vital information, such as revealing which pieces of human DNA have been favored by evolution because they confer beneficial traits -- resistance to infection or the ability to digest milk, for example. These signs can only be revealed through genetic studies of modern humans and other related species, though the task has proven difficult. </strong></div><div align="left"><strong>Now, in a paper appearing in the January 7 edition of Science Express, researchers describe a method for pinpointing these preferred regions within the human genome that offers greater precision and resolution than ever before, and the possibility of deeply understanding both our genetic past and present.<br />"It's clear that positive natural selection has been a critical force in shaping the human genome, but there are remarkably few examples that have been clearly identified," said senior author Pardis Sabeti, an associate member of the Broad Institute of Harvard and MIT and an assistant professor of organismic and evolutionary biology at Harvard University. "The method we've developed makes it possible to zero in on individual genes as well as the specific changes within them that are driving important evolutionary changes."<br />Positive natural selection is a process in which advantageous traits become more common in a population. That is because these traits boost an individual's chances of survival and reproduction, so they are readily passed on to future generations. Identifying such traits -- and the genes underlying them -- is a cornerstone of current efforts to dissect the biological history of the human species as well as the diseases that threaten human health today.<br />"In the human genome, positive natural selection leaves behind very distinctive signals," said co-first author Sharon Grossman, a research assistant at Harvard University and the Broad Institute. Yet earlier methods for detecting these signals are limited, highlighting relatively large chunks of the genome that are hundreds of thousands to millions of genetic letters or "bases" in length, and that can contain many genes.<br />Of the hundreds of these large genomic regions thought to be under positive natural selection in humans, only a handful have so far been winnowed to a precise genetic change. "Finding the specific genetic changes that are under selection can be like looking for a needle in a haystack," said Grossman.<br />Sabeti, Grossman and their colleagues wondered if there might be a way to enhance this genomic search. Because existing methods for detecting natural selection each measure distinct genomic features, the researchers predicted that an approach that combines them together could yield even better results.<br />After some initial simulations to test their new method, the research team applied it to more than 180 regions of the human genome that are thought to be under recent positive selection, yet in most cases, the specific gene or genetic variant under selection is unknown.<br />The researchers' method, called "Composite of Multiple Signals" or CMS, enabled them to dramatically narrow the size of the candidate regions, reducing them from an average of eight genes per region to one. Moreover the number of candidate genetic changes was reduced from thousands to just a handful, helping the researchers tease out the needles from the haystack.<br />"The list of genes and genetic loci we identified includes many intriguing candidates to follow up," said co-first author Ilya Shylakhter, a computational biologist at the Broad Institute and Harvard University. "For example, a number of genes identified are involved in metabolism, skin pigmentation and the immune system."<br />In some cases, the researchers were able to identify a specific genetic change that is the likely focal point of natural selection. For example, a variation in a gene called protocadherin 15, which functions in sensory perception, including hearing and vision, appears to be under selection in some East Asian populations. Several other genes involved in sensory perception also appear to be under selection in Asia. In addition, the team uncovered strong evidence of selection in East Asians at a specific point within the leptin receptor gene, which is linked to blood pressure, body mass index and other important metabolic functions.<br />Interestingly, the researchers also localized signals to regions outside of genes, suggesting that they function not by altering gene structure per se, but by changing how certain genes are turned on and off.<br />While the findings in the Science paper offer a deep glimpse of evolution's handiwork, the researchers emphasize that further studies of individual genetic variations, involving experiments that explore how certain genetic changes influence biological function, are necessary to fully dissect the role of natural selection and its impact on human biology.<br />"This method allows us to trace evolution's footprints with a much finer level of granularity than before, but it's one piece of a much larger puzzle," said Sabeti. "As more data on human genetic variation becomes available in the coming years, an even more detailed evolutionary picture should emerge." </strong></div><div align="left"><strong>Story Source:<br />Adapted from materials provided by </strong><a class="blue" href="http://www.broad.mit.edu/" rel="nofollow"><strong>Broad Institute of MIT and Harvard</strong></a><strong>, via </strong><a href="http://www.eurekalert.org/" rel="nofollow"><strong>EurekAlert!</strong></a><strong>, a service of AAAS. </strong></div><div align="left"><strong>Journal Reference:<br />Grossman et al. A composite of multiple signals distinguishes causal variants in regions of positive selection. Science, 2010 DOI: </strong><a href="http://dx.doi.org/10.1126/science.1183863" rel="nofollow"><strong>10.1126/science.1183863</strong></a><strong> </strong></div>olosciencehttp://www.blogger.com/profile/07007258673266741468noreply@blogger.com0tag:blogger.com,1999:blog-4305283407805626298.post-65260932073394927072010-01-10T01:20:00.001-08:002010-01-10T01:22:47.440-08:00What Came First in the Origin of Life? New Study Contradicts the 'Metabolism First' Hypothesis.<div align="center"><a href="http://www.sciencedaily.com/images/2010/01/100108101433.jpg"><img style="TEXT-ALIGN: center; MARGIN: 0px auto 10px; WIDTH: 300px; DISPLAY: block; HEIGHT: 225px; CURSOR: hand" border="0" alt="" src="http://www.sciencedaily.com/images/2010/01/100108101433.jpg" /></a><strong> Source: </strong><a href="http://www.sciencedaily.com/releases/2010/01/100108101433.htm"><strong><span style="color:#ffff66;">ScienceDaily</span></strong></a></div><div align="center"><strong>----------------------------</strong></div><div align="left"><strong>ScienceDaily (Jan. 9, 2010) — A new study published in Proceedings of National Academy of Sciences rejects the theory that the origin of life stems from a system of self-catalytic molecules capable of experiencing Darwinian evolution without the need of RNA or DNA and their replication. </strong></div><div align="left"><strong>The research, which was carried out with the participation of Mauro Santos, researcher of the Department of Genetics and Microbiology at Universitat Autònoma de Barcelona (UAB), has demonstrated that, through the analysis of what some researchers name "compound genomes," these chemical networks cannot be considered evolutionary units because they lose properties which are essential for evolution when they reach a critical size and greater level of complexity.<br />The U.S. National Aeronautics and Space Administration (NASA) defines life as a "self-sustaining chemical system capable of Darwinian evolution." The scientific theories on the origin of life revolve around two main ideas: one focuses on genetics -- with RNA or DNA replication as an essential condition for Darwinian evolution to take place -- and the other focuses on metabolism. It is clear that both situations must have begun with simple organic molecules formed by prebiotic processes, as was demonstrated by the Miller-Urey experiment (in which organic molecules were created from inorganic substances). The point in which these two theories differ is that the replication of RNA or DNA molecules is a far too complex process which requires a correct combination of monomers within the polymers to produce a molecular chain resulting from the replication.<br />Until now no plausible chemical explanation exists for how these processes occured. In addition, defenders of the second theory argue that the processes needed for evolution to take place depend on primordial metabolism. This metabolism is believed to be a type of chemical network entailing a high degree of mutual catalysis between its components which, in turn, eventually allows for adaptation and evolution without any molecular replication.<br />In the first half of the 20th century, Alexander Oparin established the "Metabolism First" hypothesis to explain the origin of life, thus strengthening the primary role of cells as small drops of coacervates (evolutionary precursors of the first prokaryote cells). Dr Oparin did not refer to RNA or DNA molecules since at that time it was not clear just how important the role of these molecules was in living organisms. However he did form a solid base for the idea of self-replication as a collective property of molecular compounds.<br />Science more recently demonstrated that sets of chemical components store information about their composition which can be duplicated and transmitted to their descendents. This has led to their being named "compound genomes" or composomes. In other words, heredity does not require information in order to be stored in RNA or DNA molecules. These "compound genomes" apparently fulfil the conditions required to be considered evolutionary units, which suggests a pathway from pre-Darwinian dynamics to a minimum protocell.<br />Researchers in this study nevertheless reveal that these systems are incapable of undergoing a Darwinian evolution. For the first time a rigorous analysis was carried out to study the supposed evolution of these molecular networks using a combination of numerical and analytical simulations and network analysis approximations. Their research demonstrated that the dynamics of molecular compound populations which divide after having reached a critical size do not evolve, since during this process the compounds lose properties which are essential for Darwinian evolution.<br />Researchers concluded that this fundamental limitation of "compound genomes" should lead to caution towards theories that set metabolism first as the origin as life, even though former metabolic systems could have offered a stable habitat in which primitive polymers such as RNA could have evolved.<br />Researchers state that different prebiotic Earth scenarios can be considered. However, the basic property of life as a system capable of undergoing Darwinian evolution began when genetic information was finally stored and transmitted such as occurs in nucleotide polymers (RNA and DNA). </strong></div><div align="left"><strong>Story Source:<br />Adapted from materials provided by </strong><a class="blue" href="http://www.uab.es/" rel="nofollow" target="_blank"><strong>Universitat Autonoma de Barcelona</strong></a><strong>. </strong></div><div align="left"><strong>Journal Reference:<br />Vera Vasasa, Eörs Szathmáry and Mauro Santosa. Lack of evolvability in self-sustaining autocatalytic networks: A constraint on the metabolism-first path to the origin of life. PNAS, January 4, 2010 DOI: </strong><a href="http://dx.doi.org/10.1073/pnas.0912628107" rel="nofollow" target="_blank"><strong>10.1073/pnas.0912628107</strong></a><strong> </strong></div>olosciencehttp://www.blogger.com/profile/07007258673266741468noreply@blogger.com0tag:blogger.com,1999:blog-4305283407805626298.post-30728421330410552432009-10-05T06:35:00.000-07:002009-10-05T06:37:12.024-07:00Understanding A Cell's Split Personality Aids Synthetic Circuits.<div align="center"><a href="http://www.sciencedaily.com/releases/2009/10/091004141142.htm"><img style="TEXT-ALIGN: center; MARGIN: 0px auto 10px; WIDTH: 300px; DISPLAY: block; HEIGHT: 224px; CURSOR: hand" border="0" alt="" src="http://www.sciencedaily.com/images/2009/10/091004141142.jpg" /> <strong><span style="color:#ffff66;">SOURCE</span></strong></a><br /><strong><span style="color:#ffff66;"></span></strong><br /><div align="left"><strong>ScienceDaily (Oct. 5, 2009) — As scientists work toward making genetically altered bacteria create living "circuits" to produce a myriad of useful proteins and chemicals, they have logically assumed that the single-celled organisms would always respond to an external command in the same way. </strong></div><div align="left"><strong>Alas, some bacteria apparently have an individualistic streak that makes them zig when the others zag.<br />A new set of experiments by Duke University bioengineers has uncovered the existence of "bistability," in which an individual cell has the potential to live in either of two states, depending on which state it was in when stimulated.<br />Taking into account the effects of this phenomenon should greatly enhance the future efficiency of synthetic circuits, said biomedical engineer Lingchong You of Duke's Pratt School of Engineering and the Duke Institute for Genome Sciences & Policy.<br />In principle, re-programmed bacteria in a synthetic circuit can be useful for producing proteins, enzymes or chemicals in a coordinated way, or even delivering different types of drugs or selectively killing cancer cells, the scientists said.<br />Researchers in this new field of synthetic biology "program" populations of genetically altered bacteria to direct their actions in much the same way that a computer program directs a computer. In this analogy, the genetic alteration is the software, the cell the computer. The Duke researchers found that not only does the software drive the computer's actions, but the computer in turn influences the running of the software.<br />"In the past, synthetic biologists have often assumed that the components of the circuit would act in a predictable fashion every time and that the cells carrying the circuit would just serve as a passive reactor," You said. "In essence, they have taken a circuit-centric view for the design and optimization process. This notion is helpful in making the design process more convenient."<br />But it's not that simple, say You and his graduate student Cheemeng Tan, who published the results of their latest experiments early online in the journal Nature Chemical Biology.<br />"We found that there can be unintended consequences that haven't been appreciated before," said You. "In a population of identical cells, some can act one way while others act in another. However, this process appears to occur in a predictable manner, which allows us to take into account this effect when we design circuits."<br />Bistability is not unique to biology. In electrical engineering, for example, bistability describes the functioning of a toggle switch, a hinged switch that can assume either one of two positions – on or off.<br />"The prevailing wisdom underestimated the complexity of these synthetic circuits by assuming that the genetic changes would not affect the operation of the cell itself, as if the cell were a passive chassis," said Tan. "The expression of the genetic alteration can drastically impact the cell, and therefore the circuit.<br />"We now know that when the circuit is activated, it affects the cell, which in turn acts as an additional feedback loop influencing the circuit," Tan said. "The consequences of this interplay have been theorized but not demonstrated experimentally."<br />The scientists conducted their experiments using a genetically altered colony of the bacteria Escherichia coli (E.coli) in a simple synthetic circuit. When the colony of bacteria was stimulated by external cues, some of the cells went to the "on" position and grew more slowly, while the rest went to the "off" position and grew faster.<br />"It is as if the colony received the command not to expand too fast when the circuit is on," Tan explained. "Now that we know that this occurs, we used computer modeling to predict how many of the cells will go to the 'on' or 'off' state, which turns out to be consistent with experimental measurements"<br />The experiments were supported by the National Science Foundation, the National Institutes of Health and a David and Lucille Packard Fellowship. Duke's Philippe Marguet was also a member of the research team.<br />Adapted from materials provided by </strong><a class="blue" href="http://www.duke.edu/" rel="nofollow" target="_blank"><strong>Duke University</strong></a><strong>, via </strong><a href="http://www.eurekalert.org/" rel="nofollow" target="_blank"><strong>EurekAlert!</strong></a><strong>, a service of AAAS. </strong></div></div>olosciencehttp://www.blogger.com/profile/07007258673266741468noreply@blogger.com0tag:blogger.com,1999:blog-4305283407805626298.post-44371438340758220382009-09-28T12:30:00.001-07:002009-09-28T12:32:00.073-07:00New Method For Improving The Functional Characteristics Of Enzymes.<div align="center"><a href="http://www.sciencedaily.com/releases/2009/09/090924101117.htm"><img style="TEXT-ALIGN: center; MARGIN: 0px auto 10px; WIDTH: 300px; DISPLAY: block; HEIGHT: 167px; CURSOR: hand" border="0" alt="" src="http://www.sciencedaily.com/images/2009/09/090924101117.jpg" /><br /></a><a href="http://www.sciencedaily.com/releases/2009/09/090924101117.htm"><strong><span style="color:#ffff66;">SOURCE</span></strong></a><br /><strong><span style="color:#ffff66;"></span></strong><br /><div align="left"><strong>ScienceDaily (Sep. 28, 2009) — An international team of scientists from the Czech Republic, Germany and Japan have developed a new method for improving the properties of enzymes. The method has potential for wide application in the chemical, medicinal and food industries. The research has been published in Nature Chemical Biology. </strong></div><div align="left"><strong>The modified enzymes can be used, for example, for disposal of highly harmful chemical substances which enter into the environment as a result of human activity and can have a very negative influence on human and animal health. Nature cannot degrade many of these chemicals but, in this work, the scientists have developed an approach that can be applied to remove them efficiently from the environment.<br />The principle of the discovery is based on genetic manipulation of the enzyme which is starting and accelerating the chemical reaction. „Now we can use genetic modifications for changing the properties of the enzymes so they can faster and more easily dispose of harmful substances in the environment,” says Jiri Damborsky, leader of the Protein Engineering Group at the Institute of Experimental Biology, Faculty of Science, Masaryk University.<br />Up to now, the scientists had focused during the modification of an enzyme’s properties on the site in its structure where the chemical reaction happens, the active site. The new method is based on the modification of so-called access tunnels that connect the active site with the surface of the enzyme. “Specialized computational techniques guided the experimental work to engineer these tunnels to alter their accessibility to the degraded substances,” notes Rebecca Wade, leader of the Molecular and Cellular Modeling Group at EML Research in Heidelberg.<br />The scientists applied the approach by modifying an enzyme to degrade the highly toxic substance, trichloropropane (TCP). This colourless liquid is a secondary product of chemical production. It can reside in the soil and groundwater for over 100 years, can contaminate drinking water and is a carcinogen. Using the new approach, the protein engineers developed a modified enzyme capable of degrading this substance 32 times faster than the original enzyme.<br />But the method has much wider scope for application than just in the fight against harmful substances and in environmental protection. The targeted modification of the tunnels in enzymes can be utilized in different application areas, including biomedicine, and the chemical and food industries.<br />Journal reference:<br />Martina Pavlova et al. Redesigning dehalogenase access tunnels as a strategy for degrading an anthropogenic substrate. Nature Chemical Biology, 5, 727 - 733 (2009); Published online 23 August 2009 DOI: </strong><a href="http://dx.doi.org/10.1038/nchembio.205" rel="nofollow" target="_blank"><strong>10.1038/nchembio.205</strong></a><br /><strong>Adapted from materials provided by </strong><a class="blue" href="http://www.eml.villa-bosch.de/" rel="nofollow" target="_blank"><strong>European Media Laboratory (EML)</strong></a><strong>, via </strong><a href="http://www.alphagalileo.org/" rel="nofollow" target="_blank"><strong>AlphaGalileo</strong></a><strong>. </strong></div></div>olosciencehttp://www.blogger.com/profile/07007258673266741468noreply@blogger.com1tag:blogger.com,1999:blog-4305283407805626298.post-51275367313055475402009-09-26T01:27:00.000-07:002009-09-26T01:29:48.440-07:00Yale engineers have for the first time observed and tracked E. coli bacteria moving in a liquid medium with a particular motion.<div align="center"><a href="http://www.sciencedaily.com/images/2009/09/090925115455.jpg"><img style="TEXT-ALIGN: center; MARGIN: 0px auto 10px; WIDTH: 300px; DISPLAY: block; HEIGHT: 822px; CURSOR: hand" border="0" alt="" src="http://www.sciencedaily.com/images/2009/09/090925115455.jpg" /></a> <a href="http://www.sciencedaily.com/releases/2009/09/090925115455.htm"><strong><span style="color:#ffff66;">SOURCE</span></strong></a></div><div align="center"><strong></strong> </div><div align="left"><strong>ScienceDaily (Sep. 26, 2009) — Yale engineers have for the first time observed and tracked E. coli bacteria moving in a liquid medium with a motion similar to that of a kayak paddle. </strong></div><div align="left"><strong>Their findings, which appear online September 29 in the journal Physical Review Letters, will help lead to a better understanding of how bacteria move from place to place and, potentially, how to keep them from spreading.<br />Scientists have long theorized that the cigar-shaped cell bodies of E. coli and other microorganisms would follow periodic orbits that resemble the motion of a kayak paddle as they drift downstream in a current. Until now, no one had managed to directly observe or track those movements.<br />Hur Koser, associate professor at Yale's School of Engineering & Applied Science, previously discovered that hydrodynamic interactions between the bacteria and the current align the bacteria in a way that allows them to swim upstream. "They find the most efficient route to migrate upstream, and we ultimately want to understand the mechanism that allows them to do that," Koser said.<br />In the new study, Koser, along with postdoctoral associate and lead author of the paper, Tolga Kaya, devised a method to see this motion in progress. They used advanced computer and imaging technology, along with sophisticated new algorithms, that allowed them to take millions of high-resolution images of tens of thousands of individual, non-flagellated E. coli drifting in a water and glycerin solution, which amplified the bacteria's paddle-like movements.<br />The team characterized the bacteria's motion as a function of both their length and distance from the surface. The team found that the longer and closer to the surface they were, the slower the E. coli "paddled."<br />It took the engineers months to perfect the intricate camera and computer system that allowed them to take 60 to 100 sequential images per second, then automatically and efficiently analyze the huge amount of resulting data.<br />E. coli and other bacteria can colonize wherever there is water and sufficient nutrients, including the human digestive tract. They encounter currents in many settings, from riverbeds to home plumbing to irrigation systems for large-scale agriculture.<br />"Understanding the physics of bacterial movement could potentially lead to breakthroughs in the prevention of bacterial migration and sickness," Koser said. "This might be possible through mechanical means that make it more difficult for bacteria to swim upstream and contaminate water supplies, without resorting to antibiotics or other chemicals."<br />Adapted from materials provided by </strong><a class="blue" href="http://www.yale.edu/" rel="nofollow" target="_blank"><strong>Yale University</strong></a><strong>, via </strong><a href="http://www.eurekalert.org/" rel="nofollow" target="_blank"><strong>EurekAlert!</strong></a><strong>, a service of AAAS. </strong></div>olosciencehttp://www.blogger.com/profile/07007258673266741468noreply@blogger.com0tag:blogger.com,1999:blog-4305283407805626298.post-18862693479613477792009-09-20T01:20:00.000-07:002009-09-20T01:23:02.122-07:00Mechanism Related To Onset Of Various Genetic Diseases Revealed<div align="center"><a href="http://www.sciencedaily.com/releases/2009/09/090917111615.htm"><img style="TEXT-ALIGN: center; MARGIN: 0px auto 10px; WIDTH: 300px; DISPLAY: block; HEIGHT: 236px; CURSOR: hand" border="0" alt="" src="http://www.sciencedaily.com/images/2009/09/090917111615.jpg" /> <strong><span style="color:#ffff66;">SOURCE</span></strong></a></div><div align="center"><strong><br /></strong></div><div align="left"><strong>ScienceDaily (Sep. 17, 2009) — Researchers at the Department of Biochemistry and Molecular Biology of Universitat Autònoma de Barcelona (UAB) have revealed the process by which proteins with a tendency to cause conformational diseases such as amyotrophic lateral sclerosis, familial amyloidotic polyneuropathy, familial amyloidotic cardiomyopathy, etc. finally end up causing them. </strong></div><div align="left"><strong>Researchers have carried out an analysis of their 3D structure and studied why these proteins finally become toxic although they are correctly folded, an indicator that they are functioning correctly. The answer can be found in the separation of the proteins, which under normal conditions are found in groups of two or more, caused by a genetic mutation in their composition. Researchers believe this discovery, published recently in the journal PLoS Computational Biology, could also be the cause of other diseases of unknown origins.<br />Every day cells produce thousands of new proteins which renew themselves every second and which, by obeying the orders prescribed in our genetic code, work towards the proper functioning of our body. However, these proteins occasionally suffer genetic mutations which can cause changes in their composition, thus preventing them from carrying out their functions and the activities they are assigned. In many cases this gives way to the formation of toxic macromolecular aggregates - amyloid fibrils - which block our body's protein quality control system and finally provoke cell death.<br />Protein aggregation and the misfolding of proteins can be linked to the origin of many conformational diseases which can be either genetic or spontaneous. The proteins involved can either have an unstructured or lineal unfolded form such as in Alzheimer's and Parkinson's disease or Type II Diabetes, or can be globular, showing a folded 3D-structure. The former have been widely characterised by scientists and the process by which they unfold is known. The process leaves regions uncovered which are in the risk of becoming aggregated and these eventually form toxic assemblies. Globular proteins are known to be linked to hepatic, cardiac, renal and neurological disorders. However scientists do not know exactly how they manage to aggregate despite the fact that they are correctly folded within the body.<br />Through computational analysis, researchers Salvador Ventura and Virgínia Castillo, from the UAB Department of Biochemistry and Molecular Biology, have discovered that, in non-disease conditions, globular proteins related to conformational diseases are found associated in pairs to other proteins or in complex subunits, in a way that one protein covers the aggregation-prone region of the other and thus prevents the onset of this process. Therefore these regions remain obscured in the interior of the structure and are inoffensive to the organism as long as the two proteins are joined together. Researchers have found that genetic mutations produced in the interaction sites of the protein pair prevents their association, leaving aggregation-prone regions uncovered and favouring the formation of toxic aggregates. According to researchers, this would explain why out of two people with the same globular proteins and the same risk regions, only the one who suffers a genetic mutation would finally develop a disease.<br />The conclusions obtained have led researchers to contemplate the possibility that dissociation is a general mechanism, which not only affects globular proteins with a clearly defined structure, but also others which have not yet been characterised and which could be the cause of diseases of unknown origin.<br />As possible strategies to prevent the dissociation of proteins, the authors propose introducing genetic mutations into the proteins to strengthen their association and developing specific molecules to block the risk regions of already dissociated proteins.<br />The results of the study carried out by UAB researchers coincides with those obtained by researchers at Cambridge University, who also published similar data in the journal Proceedings of the National Academic of Sciences.<br />In the future UAB researchers are planning to expand their computational analysis to cover the whole set of human proteins with a defined 3D-structure. With this objective they seek to discover the proteins responsible for different genetic diseases of unknown origins and offer a series of new therapeutic targets for these disorders.<br />Journal reference:<br />Castillo V, Ventura S. Amyloidogenic Regions and Interaction Surfaces Overlap in Globular Proteins Related to Conformational Diseases. PLoS Computational Biology, 2009; 5 (8): e1000476 DOI: </strong><a href="http://dx.doi.org/10.1371/journal.pcbi.1000476" rel="nofollow" target="_blank"><strong>10.1371/journal.pcbi.1000476</strong></a><br /><strong>Adapted from materials provided by </strong><a class="blue" href="http://www.uab.es/" rel="nofollow" target="_blank"><strong>Universitat Autonoma de Barcelona</strong></a><strong>, via </strong><a href="http://www.eurekalert.org/" rel="nofollow" target="_blank"><strong>EurekAlert!</strong></a><strong>, a service of AAAS. </strong></div>olosciencehttp://www.blogger.com/profile/07007258673266741468noreply@blogger.com0tag:blogger.com,1999:blog-4305283407805626298.post-63814193757627970892009-09-12T00:20:00.000-07:002009-09-12T00:34:00.595-07:00Frontiers of Biomedical Engineering with Prof. Mark Saltzman (Yale University)<object width="560" height="340"><param name="movie" value="http://www.youtube.com/v/Sn0bOX5Hau4&hl=en&fs=1&"></param><param name="allowFullScreen" 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width="560" height="340"></embed></object>olosciencehttp://www.blogger.com/profile/07007258673266741468noreply@blogger.com0tag:blogger.com,1999:blog-4305283407805626298.post-9115112430770416752009-07-22T08:23:00.001-07:002009-07-22T08:24:54.367-07:00Growing Sea Lamprey Embryos Dramatically Alter Genomes, Discard Millions Of Units Of DNA<div align="center"><a href="http://www.sciencedaily.com/images/2009/07/090720163734.jpg"><img style="TEXT-ALIGN: center; MARGIN: 0px auto 10px; WIDTH: 300px; DISPLAY: block; HEIGHT: 297px; CURSOR: hand" border="0" alt="" src="http://www.sciencedaily.com/images/2009/07/090720163734.jpg" /></a><span style="color:#ffff66;"> </span><strong><a href="http://www.sciencedaily.com/releases/2009/07/090720163734.htm"><span style="color:#ffff66;">SOURCE</span><br /></a></strong><br /><div align="left">ScienceDaily (July 21, 2009) — Researchers have discovered that the sea lamprey, which emerged from jawless fish first appearing 500 million years ago, dramatically remodels its genome. Shortly after a fertilized lamprey egg divides into several cells, the growing embryo discards millions of units of its DNA.</div><div align="left">The findings were published this month in the Proceedings of the National Academy of Sciences. The lead author is Jeramiah Smith, a postdoctoral fellow in genome sciences at the University of Washington (UW) working in the Benaroya Research Institute laboratory of Chris Amemiya, who is also a UW affiliate professor of iology.<br />Theirs is believed to be the first recorded observation of a vertebrate -- an animal with a spinal column -- extensively reorganizing its genome as a normal part of development. A few invertebrate species, like some roundworms, have been shown to undergo extensive genome remodeling. However, stability was thought to be vital in vertebrates' genomes to assure their highly precise, normal functioning. Only slight modifications to allow for immune response were believed to occur in the vertebrate genome, not broad-scale rearrangements.<br />Smith, Amemiya and their research team inadvertently discovered the dynamic transformations in the sea lamprey genome while studying the genetic origins of its immune system. The researchers were trying to deduce how the sea lamprey employs a copy-and-paste mechanism to generate diverse receptors for detecting a variety of pathogens.<br />The researchers were surprised to notice a difference between the genome structure in the germline -- the cells that become eggs and the sperm that fertilize them -- and the genome structure in the resulting embryonic cells. The DNA in the early embryonic cells had myriad breaks that resembled those in dying cells …but the cells weren't dying. The embryonic cells had considerably fewer repeat DNA sequences than did the sperm cells and their precursors.<br />"The remodeling begins at the point when the embryo turns on its own genes and no longer relies on its mom's store of mRNA," said Smith.<br />The restructuring doesn't occur all at once, but continues for a long while during embryonic development. It took at lot of work for the scientists to see what was lost and when. They learned, among other findings, that the remodeled genome had fewer repeats and specific gene-encoding sequences. Deletions along the strands of DNA are also thought to move certain regulatory switches in the genome closer to previously distant segments.<br />The scientists don't know how this happens, or why. Smith said that his favorite hypothesis, yet unproven, is that the extra genetic material might play a role in the proliferation of precursor cells for sperm and eggs, and in early embryonic development. The genetic material might then be discarded either when it is no longer needed or to prevent abnormal growth.<br />The alteration of the sea lamprey genome and of invertebrates that restructure their genome appears to be tightly regulated, according to Smith, yet the resulting structural changes seem almost like the DNA errors that give rise to cancers or other genomic disorders in higher animals. Learning how sea lamprey DNA rearrangements are regulated during development might provide information on what stabilizes or changes the genome, he said, as well the role of restructuring in helping form different types of body cells, like fin, muscle, or liver cells.<br />If 20 percent of their genome disappears, how do sea lampreys pass along the full complement of their genes to their offspring?<br />"The germline -- those precursor cells for sperm and eggs -- is a continuous lineage through time," Smith explained. "The precursor cells for sperm and egg are set apart early in lamprey development. The genome in that cell population should never change." Genetic material is assumed to be lost only in the early embryonic cells destined to become body parts and not in cells that give rise to the next generation. The researchers have been looking for the primordial stem cells for sperm and eggs hidden away in the lamprey, but they are difficult to find.<br />Researchers do not yet know how the sea lamprey's genome guides the morphing it undergoes during its life. Sea lampreys have a long juvenile life as larvae in fresh water, where they eat on their own. Their short adult lives are normally spent in the sea as blood-sucking parasites. Their round, jawless mouths stick like suction cups to other fish. Several circular rows of teeth rasp through the skin of their unlucky hosts. Their appetite is voracious.<br />Later, as they return to streams and rivers along the northern Atlantic seaboard, sea lampreys atrophy until they are little more than vehicles for reproduction. After mating, they perish. Populations of sea lamprey were landlocked in the Great Lakes and other nearby large lakes after canals and dams were built in the early 1900's. They thrive by parasitizing (and killing) commercially important fish species and are considered a nuisance in the Great Lakes region.<br />Biologists are interested in the sea lamprey partly because of its alternating lifestyles, but largely because it represents a living fossil from around the time vertebrates originated. Close relatives of sea lampreys were on earth before the dinosaurs. It's possible that the sea lamprey's dynamic genome biology might someday be traced back in evolutionary history to a point near, and perhaps including, a common ancestor of all vertebrates living today, the authors of the study noted.<br />"Sea lampreys have a half billion years of evolutionary history," Smith said. "Evolutionary biologists and geneticists can compare their genomes to other vertebrates and humans to see what parts of the lamprey genome might have been present in our primitive ancestors. We might begin to understand how changes in the sea lamprey genome led to their distinct body structure and how fishes evolved from jawless to jawed."<br />Amemiya added, "We don't really know where this discovery about the sea lamprey's remodeling of its genome will take us. It's common in science for the implications of a finding not to be realized for several decades. It's less about connecting the dots to a specific application, and more about obtaining a broad understanding of how living things are put together."<br />In addition to Smith and Amemiya, the other researchers on this study were Francesca Antonacci and Evan E. Eichler of the UW Department of Genome Sciences. Research grants from the National Institutes of Health,the National Science Foundation and the Howard Hughes Medical Institute funded the project. Smith also received National Research Service Awards, including an Institutional Ruth L. Krischstein Award through the University of Washington Department of Genome Sciences and an individual Ruth L. Krischstein Award through the National Institute of General Medical Sciences.<br />Adapted from materials provided by <a class="blue" href="http://www.washington.edu/" rel="nofollow" target="_blank">University of Washington</a>. </div></div>olosciencehttp://www.blogger.com/profile/07007258673266741468noreply@blogger.com0tag:blogger.com,1999:blog-4305283407805626298.post-69852814501499269232009-07-17T02:19:00.001-07:002009-07-17T02:21:33.925-07:00How Staph Infections Alter Immune System<div align="center"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEg0hXZ07nOhaAsrqSVj2VA_FxccGDxlzJdZcsl-0NiowWOOg-65gQYWbZCHWm8jajl2b0ZubA0ArTs3ihQVwHf2sVjwQBShARyBa6PVcFqNzLH6V-D09dcT81Ax0TfthMLxbHxIBZR7OBA/s1600-h/CELLULE.jpg"><img style="TEXT-ALIGN: center; MARGIN: 0px auto 10px; WIDTH: 320px; DISPLAY: block; HEIGHT: 252px; CURSOR: hand" id="BLOGGER_PHOTO_ID_5359356458287843186" border="0" alt="" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEg0hXZ07nOhaAsrqSVj2VA_FxccGDxlzJdZcsl-0NiowWOOg-65gQYWbZCHWm8jajl2b0ZubA0ArTs3ihQVwHf2sVjwQBShARyBa6PVcFqNzLH6V-D09dcT81Ax0TfthMLxbHxIBZR7OBA/s320/CELLULE.jpg" /></a><span style="color:#ffff66;"> </span><a href="http://www.sciencedaily.com/releases/2009/07/090714085816.htm"><strong><span style="color:#ffff66;">SOURCE</span></strong></a></div><div align="center"><br /></div><div align="left">ScienceDaily (July 17, 2009) — Infectious disease specialists at UT Southwestern Medical Center have mapped the gene profiles of children with severe Staphylococcus aureus infections, providing crucial insight into how the human immune system is programmed to respond to this pathogen and opening new doors for improved therapeutic interventions. </div><div align="left">In recent years, much research has focused on understanding precisely what the bacterium S. aureus does within the host to disrupt the immune system. Despite considerable advances, however, it remained unclear how the host's immune system responded to the infection and why some people are apt to get more severe staphylococcal infections than others.<br />By using gene expression profiling, a process that summarizes how individual genes are being activated or suppressed in response to the infection, UT Southwestern researchers pinpointed how an individual's immune system responds to a S. aureus infection at the genetic level.<br />"The beauty of our study is that we were able to use existing technology to understand in a real clinical setting what's going on in actual humans – not models, not cells, not mice, but humans," said Dr. Monica Ardura, instructor of pediatrics at UT Southwestern and lead author of the study available online in PLoS One. "We have provided the first description of a pattern of response within an individual's immune system that is very consistent, very reproducible and very intense."<br />The immune system consists of two components: the innate system, which provides immediate defense against infection; and the adaptive system, whose memory cells are called into action to fight off subsequent infections.<br />In this study, researchers extracted ribonucleic acid from a drop of blood and placed it on a special gene chip called a microarray, which probes the entire human genome to determine which genes are turned on or off. They found that in children with invasive staphylococcal infections, the genes involved in the body's innate immune response are overactivated while those associated with the adaptive immune system are suppressed.<br />"It's a very sophisticated and complex dysregulation of the immune system, but our findings prove that there's consistency in the immune response to the staphylococcus bacterium," Dr. Ardura said. "Now that we know how the immune system responds, the question is whether we can use this to predict patient outcomes or differentiate the sickest patients from the less sick ones. How can we use this knowledge to develop better therapies?"<br />Researchers used blood samples collected between 2001 and 2005 from 77 children – 53 hospitalized at Children's Medical Center Dallas with invasive S. aureus infections and 24 controls. The control samples were collected from healthy children attending either well-child clinic or undergoing elective surgical procedures. Children with underlying chronic diseases, immunodeficiency, multiple infections, and those who received steroids or other immunomodulatory therapies were excluded from the study.<br />The children ranged in age from a few months to 15 years and included 43 boys and 34 girls. Those with S. aureus infections – both methicillin-resistant (MRSA) and methicillin-susceptible (MSSA) – were matched with healthy controls for age, sex and race. The researchers also characterized the extent as well as the type of infection in each patient to make sure that the strain of bacteria didn't influence the results.<br />Dr. Ardura stressed that more research is needed because the results represent a one-time snapshot of what's going on in the cell during an invasive staphylococcal infection.<br />"The median time to get the blood sample was day four because we wanted to make sure the hospitalized children had a S. aureus infection, and its takes four days to have final identification of the bacterial pathogen," she said.<br />The next step, Dr. Ardura said, is to study those dynamics in patients before, during and after infection. They also hope to understand better how various staph-infection therapies affect treatment.<br />"This is a very important proof-of-concept that the information is there for us to grab," Dr. Ardura said. "Now we have to begin to understand what that data tells us."<br />The work was supported by the National Institutes of Health, the Center for Lupus Research and the Baylor Health Care System Foundation.<br />Adapted from materials provided by <a class="blue" href="http://www.swmed.edu/" rel="nofollow" target="_blank">UT Southwestern Medical Center</a>, via <a href="http://www.eurekalert.org/" rel="nofollow" target="_blank">EurekAlert!</a>, a service of AAAS. </div>olosciencehttp://www.blogger.com/profile/07007258673266741468noreply@blogger.com0tag:blogger.com,1999:blog-4305283407805626298.post-52154030053347628232009-07-17T01:57:00.001-07:002009-07-17T01:59:03.239-07:00Male Sex Chromosome Losing Genes By Rapid Evolution, Study Reveals<div align="center"><a href="http://www.sciencedaily.com/releases/2009/07/090716201127.htm"><img style="TEXT-ALIGN: center; MARGIN: 0px auto 10px; WIDTH: 300px; DISPLAY: block; HEIGHT: 450px; CURSOR: hand" border="0" alt="" src="http://www.sciencedaily.com/images/2009/07/090716201127.jpg" /><strong><span style="color:#ffff66;"> SOURCE</span></strong></a></div><div align="center"><br /></div><div align="left">ScienceDaily (July 17, 2009) — Scientists have long suspected that the sex chromosome that only males carry is deteriorating and could disappear entirely within a few million years, but until now, no one has understood the evolutionary processes that control this chromosome's demise. Now, a pair of Penn State scientists has discovered that this sex chromosome, the Y chromosome, has evolved at a much more rapid pace than its partner chromosome, the X chromosome, which both males and females carry. </div><div align="left">This rapid evolution of the Y chromosome has led to a dramatic loss of genes on the Y chromosome at a rate that, if maintained, eventually could lead to the Y chromosome's complete disappearance. The research team, which includes Associate Professor of Biology Kateryna Makova, the team's leader, and National Science Foundation Graduate Research Fellow Melissa Wilson, will publish its results in the 17 July 2009 issue of the journal PLoS Genetics.<br />"There are three classes of mammals," said Makova, "egg-laying mammals, like the platypus and the echidna; marsupials, like the opossum and the wallaby; and all other mammals -- called eutherians -- which include humans, dogs, mice, and giraffes. The X and Y chromosomes of marsupials and eutherians evolved from a pair of non-sex chromosomes to become sex chromosomes."<br />Humans have 23 pairs of chromosomes, which are the structures that hold our DNA, but just one pair of these chromosomes are sex chromosomes, while the others are referred to as non-sex chromosomes. "In eutherian mammals, the sex chromosomes contain an additional region of DNA whereas, in the egg-laying mammals and marsupials, this additional region of DNA is located on the non-sex chromosomes," said Makova. "At first, bits of DNA within this additional region were readily swapped between the X and Y chromosomes, but some time between 80 and 130 million years ago, the region became two completely separate entities that no longer swapped DNA. One of the regions became specifically associated with the X chromosome and the other became specifically associated with the Y chromosome."<br />By comparing the DNA of the X and Y chromosomes in eutherian mammals to the DNA of the non-sex chromosomes in the opossum and platypus, the team was able to go back in time to the point when the X and Y chromosomes were still swapping DNA, just like the non-sex chromosomes in the opossum and platypus. The scientists then were able to observe how the DNA of the X and Y chromosomes changed over time relative to the DNA of the non-sex chromosomes. "Our research revealed that the Y-specific DNA began to evolve rapidly at the time that the DNA region split into two entities, while the X-specific DNA maintained the same evolutionary rate as the non-sex chromosomes," said Makova.<br />Once the biologists determined that the Y chromosome has been evolving more rapidly and has been losing more genes as a result, they wanted to find out why the Y chromosome has not already disappeared entirely. "Today, the human Y chromosome contains less than 200 genes, while the human X chromosome contains around 1,100 genes," said Wilson. "We know that a few of the genes on the Y chromosome are important, such as the ones involved in the formation of sperm, but we also know that most of the genes were not important for survival because they were lost, which led to the very different numbers of genes we observe between the once-identical X and Y. Although there is evidence that the Y chromosome is still degrading, some of the surviving genes on the Y chromosome may be essential, which can be inferred because these genes have been maintained for so long."<br />The team then decided to test the hypothesis that some of the genes on the Y chromosome are being maintained because they are essential. The team's approach was to compare the expression and function of genes on the Y chromosome with analogous genes on the X chromosome. "If the genes' expressions and/or functions were different, then it would make sense that the genes on the Y chromosome would be maintained because they are doing something that the genes on the X chromosome can't do," said Makova. "This hypothesis turned out to be correct."<br />Although some of the genes on the Y chromosome have been maintained, most of them have died, and the team found evidence that some others are on track to disappear, as well. "Even though some of the genes appear to be important, we still think there is a chance that the Y chromosome eventually could disappear," said Makova. "If this happens, it won't be the end of males. Instead, a new pair of non-sex chromosomes likely will start on the path to becoming sex chromosomes."<br />In the future, the team plans to use its newly generated data to create a computer model that tracks the degeneration of the Y chromosome. The scientists hope to determine how long it will take for the Y chromosome to disappear. They also hope to identify the processes that are most important for degeneration of the Y chromosome.<br />This research was funded by the National Institutes of Health, Penn State, and the National Science Foundation.<br />Adapted from materials provided by <a class="blue" href="http://www.psu.edu/" rel="nofollow" target="_blank">Penn State</a>, via <a href="http://www.eurekalert.org/" rel="nofollow" target="_blank">EurekAlert!</a>, a service of AAAS. </div>olosciencehttp://www.blogger.com/profile/07007258673266741468noreply@blogger.com0tag:blogger.com,1999:blog-4305283407805626298.post-39436357850184755242009-07-17T01:54:00.000-07:002009-07-17T01:56:37.474-07:00Handle With Care: Telomeres Resemble DNA Fragile Sites<div align="center"><a href="http://www.sciencedaily.com/images/2009/07/090710092030.jpg"><img style="TEXT-ALIGN: center; MARGIN: 0px auto 10px; WIDTH: 300px; DISPLAY: block; HEIGHT: 215px; CURSOR: hand" border="0" alt="" src="http://www.sciencedaily.com/images/2009/07/090710092030.jpg" /></a> <a href="http://www.sciencedaily.com/releases/2009/07/090710092030.htm"><strong><span style="color:#ffff66;">SOURCE</span></strong></a><br /><br /><div align="left">ScienceDaily (July 17, 2009) — Telomeres, the repetitive sequences of DNA at the ends of linear chromosomes, have an important function: They protect vulnerable chromosome ends from molecular attack. Researchers at Rockefeller University now show that telomeres have their own weakness. They resemble unstable parts of the genome called fragile sites where DNA replication can stall and go awry. But what keeps our fragile telomeres from falling apart is a protein that ensures the smooth progression of DNA replication to the end of a chromosome. </div><div align="left">The research, led by Titia de Lange, head of the Laboratory of Cell Biology and Genetics, and first author Agnel Sfeir, a postdoctoral associate in the lab, suggests a striking similarity between telomeres and common fragile sites, parts of the genome where breaks tend to occur, albeit infrequently. (Humans have 80 common fragile sites, many of which have been linked to cancer.) De Lange and Sfeir found that these newly discovered fragile sites make it difficult for DNA replication to proceed, a discovery that unveils a new replication problem posed by telomeres.<br />At the center of the discovery is a protein known as TRF1, which de Lange, in an effort to understand how telomeres protect chromosome ends, discovered in 1995. Using a conditional mouse knockout, de Lange and Sfeir have now revealed that TRF1, which is part of a six-protein complex called shelterin, enables DNA replication to drive smoothly through telomeres with the aid of two other proteins.<br />“Telomeric DNA has a repetitive sequence that can form unusual DNA structures when the DNA is unwound during DNA replication,” says de Lange. “Our data suggest that TRF1 brings in two proteins that can take out these structures in the telomeric DNA. In other words, TRF1 and its helpers remove the bumps in the road so that the replication fork can drive through.”<br />The work, published in the July 10 issue of Cell, began when Sfeir deleted TRF1 and saw that the telomeres resembled common fragile sites, suggesting that TRF1 protects telomeres from becoming fragile. Instead of a continuous string of DNA, the telomeres were broken into fragments of twos and threes. To see if the replication fork stalls at telomeres, de Lange and Sfeir joined forces with Carl L. Schildkraut, a researcher at Albert Einstein College of Medicine in New York City. Using a technique called SMARD, the researchers observed the dynamics of replication across individual DNA molecules — the first time this technique has been used to study telomeres. In the absence of TRF1, the fork often stalled for a considerable amount of time.<br />The only other known replication problem posed by telomeres was solved in 1985 when it was shown that the enzyme telomerase elongates telomeres, which shorten during every cell division. The second problem posed by telomeres, the so-called end-protection problem, was solved by de Lange and her colleagues when they found that shelterin protects the ends of linear chromosomes, which look like damaged DNA, from unnecessary repair. Working with TRF1, the very first shelterin protein ever to be identified, de Lange and Sfeir have not only unveiled a completely unanticipated replication problem at telomeres, they have also shown how it is solved.<br />The research lays new groundwork for the study of common fragile sites throughout the genome, explains de Lange. “Fragile sites have always been hard to study because no specific DNA sequence preceeds or follows them,” she says. “In constrast, telomeres represent fragile sites with a known sequence, which may help us understand how common fragile sites break throughout the genome — and why.”<br />Journal reference:<br />Agnel Sfeir, Settapong T. Kosiyatrakul, Dirk Hockemeyer, Sheila L. MacRae, Jan Karlseder, Carl L. Schildkraut and Titia de Lange. Mammalian Telomeres Resemble Fragile Sites and Require TRF1 for Efficient Replication. Cell, 138(1): 90%u2014103 (July 10, 2009) [<a href="http://www.cell.com/abstract/S0092-8674%2809%2900721-1" rel="nofollow" target="_blank">link</a>]<br />Adapted from materials provided by <a class="blue" href="http://www.rockefeller.edu/" rel="nofollow" target="_blank">Rockefeller University</a>. </div></div>olosciencehttp://www.blogger.com/profile/07007258673266741468noreply@blogger.com0tag:blogger.com,1999:blog-4305283407805626298.post-43315545288839162732009-07-17T01:35:00.000-07:002009-07-17T01:37:33.257-07:00By Manipulating Oxygen, Scientists Coax Bacteria Into Never-Before-Seen Solitary Wave<div align="center"><a href="http://www.sciencedaily.com/images/2009/07/090716134903.jpg"><img style="TEXT-ALIGN: center; MARGIN: 0px auto 10px; WIDTH: 300px; DISPLAY: block; HEIGHT: 249px; CURSOR: hand" border="0" alt="" src="http://www.sciencedaily.com/images/2009/07/090716134903.jpg" /></a> <a href="http://www.sciencedaily.com/releases/2009/07/090716134903.htm"><strong><span style="color:#ffff66;">SOURCE</span></strong></a></div><div align="center"><br /></div><div align="left">ScienceDaily (July 17, 2009) — Bacteria know that they are too small to make an impact individually. So they wait, they multiply, and then they engage in behaviors that are only successful when all cells participate in unison. There are hundreds of behaviors that bacteria carry out in such communities. Now researchers at Rockefeller University have discovered one that has never been observed or described before in a living system.</div><div align="left">In research published in the May 12 issue of Physical Review Letters, Albert J. Libchaber, head of the Laboratory of Experimental Condensed Matter Physics, and his colleagues, including first author Carine Douarche, a postdoctoral associate in the lab, show that when oxygen penetrates a sample of oxygen-deprived Escherichia coli bacteria, they do something that no living community had been seen to do before: The bacteria accumulate and form a solitary propagating wave that moves with constant velocity and without changing shape. But while the front is moving, each bacterium in it isn’t moving at all.<br />“It’s like a soliton,” says Douarche. “A self-reinforcing solitary wave.”<br />Unlike the undulating pattern of an ocean wave, which flattens or topples over as it approaches the shore, a soliton is a solitary, self-sustaining wave that behaves like a particle. For example, when two solitons collide, they merge into one and then separate into two with the same shape and velocity as before the collision. The first soliton was observed in 1834 at a canal in Scotland by John Scott Russell, a scientist who was so fascinated with what he saw that he followed it on horseback for miles and then set up a 30-foot water tank in his yard where he successfully simulated it, sparking considerable controversy.<br />The work began when Libchaber, Douarche and their colleagues placed E. coli bacteria in a sealed square chamber and measured the oxygen concentration and the density of bacteria every two hours until the bacteria consumed all the oxygen. (Bacteria, unlike humans, don’t die when starved for oxygen, but switch to a nonmotile state from which they can be revived.) The researchers then cracked the seals of the chamber, allowing oxygen to flow in.<br />The result: The motionless bacteria, which had spread out uniformly, began to move; first those around the perimeter, nearest to the seals, and then those further away. A few hours later, the bacteria began to spatially segregate into two domains of moving and nonmoving bacteria and pile up into a ring at the border of low-oxygen and no-oxygen. There they formed a solitary wave that propagated slowly but steadily toward the center of the chamber without changing its shape.<br />The effect, which lasted for more than 15 hours and covered a considerable distance (for bacteria), could not be explained by the expression of new proteins or by the addition of energy in the system. Instead, the creation of the front depends on the dispersion of the active bacteria and on the time it takes for oxygen-starved bacteria to completely stop moving, 15 minutes. The former allows the bacteria to propagate at a constant velocity, while the latter keeps the front from changing shape.<br />However, a propagating front of bacteria wasn’t all that was created. “To me, the biggest surprise was that the bacteria control the flow of oxygen in the regime,” says Libchaber. “There’s a propagating front of bacteria, but there is a propagating front of oxygen, too. And the bacteria, by absorbing the oxygen, control it very precisely.”<br />Oxygen, Libchaber explains, is one of the fastest-diffusing molecules, moving from regions of high concentration to low concentration such that the greater the distance it needs to travel, the faster it will diffuse there. But that is not what they observed. Rather, oxygen penetrated the chamber very slowly in a linear manner. Equal time, equal distance. “This pattern is not due to biology,” says Libchaber. “It has to do with the laws of physics. And it is organized in such an elegant way that the only thing it tells us is that we have a lot to learn from bacteria.”<br />Journal reference:<br />Douarche et al. E. Coli and Oxygen: A Motility Transition. Physical Review Letters, 2009; 102 (19): 198101 DOI: <a href="http://dx.doi.org/10.1103/PhysRevLett.102.198101" rel="nofollow" target="_blank">10.1103/PhysRevLett.102.198101</a><br />Adapted from materials provided by <a class="blue" href="http://www.rockefeller.edu/" rel="nofollow" target="_blank">Rockefeller University</a>. </div>olosciencehttp://www.blogger.com/profile/07007258673266741468noreply@blogger.com0tag:blogger.com,1999:blog-4305283407805626298.post-36376385970459408472009-07-17T01:14:00.001-07:002009-07-17T01:16:05.586-07:00DNA Not The Same In Every Cell Of Body<div align="center"><a href="http://www.sciencedaily.com/images/2009/07/090715131449.jpg"><img style="TEXT-ALIGN: center; MARGIN: 0px auto 10px; WIDTH: 300px; DISPLAY: block; HEIGHT: 216px; CURSOR: hand" border="0" alt="" src="http://www.sciencedaily.com/images/2009/07/090715131449.jpg" /></a> <a href="http://www.sciencedaily.com/releases/2009/07/090715131449.htm"><strong><span style="color:#ffff66;">SOURCE</span></strong></a></div><div align="center"><br /></div><div align="left">ScienceDaily (July 16, 2009) — Research by a group of Montreal scientists calls into question one of the most basic assumptions of human genetics: that when it comes to DNA, every cell in the body is essentially identical to every other cell. Their results appear in the July issue of the journal Human Mutation. </div><div align="left">This discovery may undercut the rationale behind numerous large-scale genetic studies conducted over the last 15 years, studies which were supposed to isolate the causes of scores of human diseases.<br />Except for cancer, samples of diseased tissue are difficult or even impossible to take from living patients. Thus, the vast majority of genetic samples used in large-scale studies come in the form of blood. However, if it turns out that blood and tissue cells do not match genetically, these ambitious and expensive genome-wide association studies may prove to have been essentially flawed from the outset.<br />This discovery sprang from an investigation into the underlying genetic causes of abdominal aortic aneurysms (AAA) led by Dr. Morris Schweitzer, Dr. Bruce Gottlieb, Dr. Lorraine Chalifour and colleagues at McGill University and the affiliated Lady Davis Institute for Medical Research at Montreal's Jewish General Hospital. The researchers focused on BAK, a gene that controls cell death.<br />What they found surprised them.<br />AAA is one of the rare vascular diseases where tissue samples are removed as part of patient therapy. When they compared them, the researchers discovered major differences between BAK genes in blood cells and tissue cells coming from the same individuals, with the suspected disease "trigger" residing only in the tissue. Moreover, the same differences were later evident in samples derived from healthy individuals.<br />"In multi-factorial diseases other than cancer, usually we can only look at the blood," explained Gottlieb, a geneticist with McGill's Centre for Translational Research in Cancer. "Traditionally when we have looked for genetic risk factors for, say, heart disease, we have assumed that the blood will tell us what's happening in the tissue. It now seems this is simply not the case."<br />"From a genetic perspective, therapeutic implications aside, the observation that not all cells are the same is extremely important. That's the bottom line," he added. "Genome-wide association studies were introduced with enormous hype several years ago, and people expected tremendous breakthroughs. They were going to draw blood samples from thousands or hundreds of thousands of individuals, and find the genes responsible for disease.<br />"Unfortunately, the reality of these studies has been very disappointing, and our discovery certainly could explain at least one of the reasons why."<br />AAA is a localized widening and weakening of the abdominal aorta, and primarily affects elderly Caucasian men who smoke, have high blood pressure and high cholesterol levels. It often has no symptoms, but can lead to aortic ruptures which are fatal in 90 per cent of cases.<br />If the mutations discovered in the tissue cells actually predispose for AAA, they present an ideal target for new therapies, and may have even wider therapeutic implications.<br />"This will probably have repercussions for vascular disease in general," said Schweitzer, of McGill's Department of Medicine. "We have not yet looked at coronary or cerebral arteries, but I would suspect that this mutation may be present across the board."<br />Schweitzer is optimistic that this discovery may lead to new treatments for vascular disease in the near to medium term.<br />"The timeline might be five to 10 years," he said. "We have to do in-vitro cell culture experiments first, prove it in an animal model, and then develop a molecule or protein which will affect the mutated gene product. This is the first step, but it's an important step."<br />Adapted from materials provided by <a class="blue" href="http://www.mcgill.ca/" rel="nofollow" target="_blank">McGill University</a>. </div>olosciencehttp://www.blogger.com/profile/07007258673266741468noreply@blogger.com0tag:blogger.com,1999:blog-4305283407805626298.post-12531756075860242762009-07-16T01:05:00.000-07:002009-07-16T01:07:46.061-07:00Genomes Of Parasitic Flatworms Decoded<div align="center"><a href="http://www.sciencedaily.com/images/2009/07/090715131439.jpg"><img style="TEXT-ALIGN: center; MARGIN: 0px auto 10px; WIDTH: 300px; DISPLAY: block; HEIGHT: 300px; CURSOR: hand" border="0" alt="" src="http://www.sciencedaily.com/images/2009/07/090715131439.jpg" /></a> <strong><a href="http://www.sciencedaily.com/releases/2009/07/090715131439.htm">SOURCE</a></strong></div><strong><div align="center"><br /></div></strong><div align="left">ScienceDaily (July 16, 2009) — Two international research teams have determined the complete genetic sequences of two species of parasitic flatworms that cause schistosomiasis, a debilitating condition also known as snail fever. Schistosoma mansoni and Schistosoma japonicum are the first sequenced genomes of any organism in the large group called Lophotrochozoa, which includes other free-living and parasitic flatworms as well as segmented roundworms, such as the earthworm. </div><div align="left">The research was supported in part by the National Institute of Allergy and Infectious Diseases (NIAID), one of the National Institutes of Health (NIH), and is published in the current issue of Nature. The genomic information obtained through these sequencing projects suggests ways to design drugs or other compounds targeted specifically at proteins or other gene products required by the parasite to find or survive in its human or snail host.<br />"Chronic infection with Schistosoma parasites makes life miserable for millions of people in tropical countries around the globe, and can lead to death," says NIAID Director Anthony S. Fauci, M.D. Anemia, fever, fatigue and other symptoms can make it difficult for sufferers to work or go to school, he adds. "New drugs and other interventions are badly needed to reduce the impact of a disease that lowers quality of life and slows economic development."<br />People become infected with Schistosoma when they wade or bathe in water inhabited by tiny snails that are the parasite's intermediate hosts. Microscopic fork-tailed parasites released into the water by the snails burrow into a bather's skin and travel to blood vessels that supply urinary and intestinal organs, including the liver, where they mature. Female worms, which live inside the thicker males, release many thousands of eggs each day. Eggs shed in urine and feces may make their way into snail-inhabited water, where they hatch to release parasites that seek out snails to begin the cycle again.<br />Schistosomiasis cases top 200 million every year, and some 20 million people are seriously disabled by severe anemia, chronic diarrhea, internal bleeding and organ damage caused by the worms and their eggs, or the immune system reactions they provoke. Though best known for causing chronic illness, schistosomiasis also kills: In sub-Saharan Africa alone it kills some 280,000 people each year.<br />Since the 1980s, the inexpensive anti-worm medication praziquantel has been administered to people in nationwide schistosomiasis control programs in dozens of tropical countries where the disease is common. While the drug is effective, it does not prevent a person from becoming re-infected through exposure to infested waters.<br />"The mass administration of a single drug increases the chance the parasites will become resistant to it," notes Martin John Rogers, Ph.D., a program officer in NIAID's Parasitology and International Programs branch. "Reliance on one drug is not a satisfactory long-term solution to the problem of schistosomiasis."<br />Finding new drug targets was a key goal of the team that sequenced the S. masoni genome. Led by NIAID grantee Najib M. El-Sayed, Ph.D., of University of Maryland, College Park, the group determined the sequence of 363 million nucleotides, encoding 11,809 genes. Analysis of the genes and the proteins they encode revealed the loss of some types of genes (and proteins) and expansion of other gene families relative to corresponding genes found in non-parasitic worms.<br />These genetic gains and losses are tied to the parasitic lifestyle of Schistosoma. For example, the researchers detected a large percentage of genes encoding proteases (enzymes that break down proteins.) Parasites, like Schistosoma, that must bore through skin and other tissues to invade their hosts require many such enzymes. Befitting a parasite that must navigate murky waters to find its intermediate host and later must travel through several tissue types in its human host, Schistosoma flatworms have sophisticated neurosensory systems that allow them to, for example, detect chemical, light and temperature levels in water or inside their hosts. Genes that encode signaling proteins involved in these neurosensory processes made up a significant proportion of both S. masoni and S. japonicum genomes.<br />The team responsible for the S. masoni genome also used bioinformatic computational techniques to translate genetic sequence information into maps of over 600 enzymatic reactions arrayed in multiple metabolic pathways. The analysis revealed 120 flatworm enzymes that could potentially be targeted with drugs that would disable the enzyme and inhibit the parasite's metabolism.<br />Finally, in an effort to find currently marketed drugs (such as protein or enzyme inhibitors) that might also be deployed against schistosomiasis, the researchers compared information about parasite proteins to a database of drugs directed at other human diseases. They found 66 instances of currently marketed drugs that might also be effective against schistosomiasis. "This list represents a good starting point, but, of course, more research is needed to determine whether any of the compounds could also be used to treat schistosomiasis," says Dr. Rogers.<br />NIAID provided major funding for the S. masoni genome sequencing. Additional support was provided by the Wellcome Trust of Great Britain and through grants from the Fogarty International Center and the National Institute of General Medical Sciences (both components of NIH.)<br />The S. japonicum genome was produced by an international team of researchers led by Zhu Chen, Ph.D., Ze-Guang Han, Ph.D., and Shengyue Wang, Ph.D., of the Chinese National Human Genome Center, Shanghai. NIAID grantee Zheng Feng, M.D., of the Chinese Center for Disease Control and Prevention, is a coauthor on the paper.<br />Journal references:<br />M Berriman et al. The genome of the blood fluke Schistosoma mansoni. Nature, DOI: <a href="http://dx.doi.org/10.1038/nature08160" rel="nofollow" target="_blank">10.1038/nature08160</a><br />Zhou et al. The Schistosoma japonicum genome reveals features of host-parasite interplay. Nature, 2009; 460 (7253): 345 DOI: <a href="http://dx.doi.org/10.1038/nature08140" rel="nofollow" target="_blank">10.1038/nature08140</a><br />Adapted from materials provided by <a class="blue" href="http://www.niaid.nih.gov/" rel="nofollow" target="_blank">NIH/National Institute of Allergy and Infectious Diseases</a>.</div>olosciencehttp://www.blogger.com/profile/07007258673266741468noreply@blogger.com0