tag:blogger.com,1999:blog-5257447505398141232024-03-05T07:35:25.078-08:00Petrov Lab BlogThe news from the Petrov Lab at Stanford University and the blog posts by the members of the lab.Petrov Labhttp://www.blogger.com/profile/17303400627666039056noreply@blogger.comBlogger46125tag:blogger.com,1999:blog-525744750539814123.post-57628683967271026762011-12-05T11:42:00.000-08:002012-01-03T09:59:32.952-08:00Balancing selection as the natural outcome of adaptation<blockquote><b class="style1"><a href="http://www.blogger.com/post-edit.g?blogID=525744750539814123&postID=5762868396727102676" name="PNAS2011"></a></b> </blockquote><a href="http://petrov.stanford.edu/pdfs/79.pdf" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img alt="image" border="0" class="left" height="120" src="http://petrov.stanford.edu/images/Sellisetal2011.jpg" width="90" /></a>Balancing selection is often presented in opposition to directional selection. Indeed, balancing selection promotes maintenance of genetic variation while directional selection pushes one genetic variant at the expense of the other and removes natural selection from populations. Directional selection is expected to leave genomic signatures of allelic change that is too fast to be explained by the neutral theory while balancing selection is often detected as allelic changes that are too slow. It is thus to our great surprise that we discovered that this opposition might in fact be illusory. <a href="http://petrov.stanford.edu/pdfs/79.pdf">In a PNAS paper</a> by Diamantis Sellis, Benjamin Callahan, Dmitri Petrov and Philipp Messer<a href="http://petrov.stanford.edu/pdf/79.pdf"> </a>we showed that directional selection in diploids is in fact expected to generate balanced genetic variants. Both directional and balancing selection might be two sides of the same coin, both being the consequence of genetic adaptation. One way to see this is to consider that new adaptive mutations in diploids exist first as heterozygotes. Thus they need to be adaptive as heterozygotes or they would not be seen by natural selection (the so called Haldane sieve). On the other hand nothing ensures that the mutant homozygote needs to be better than the heterozygote. That is not a requirement for the invasion of the adaptive mutation. Using Fisher's phenotypic model of adaptation we showed that if one allows suficiently large mutations to occur then many adaptive mutations should show heterozygote advantage. These adaptive mutations invade the population, persist in the balanced state often for a very short period of time, and then removed due to the invasion of new adaptive mutations that are themselves often overdominant. We argue that balancing selection might be widespread, that balanced alleles do not need to be old as often presumed, and that adaptation might be a force that promotes rather than exhausts genetic variation.Petrov Labhttp://www.blogger.com/profile/17303400627666039056noreply@blogger.com0tag:blogger.com,1999:blog-525744750539814123.post-43054046053217401582011-08-01T11:48:00.000-07:002012-01-03T16:31:15.639-08:00Faster than neutral evolution of constrained sequences<blockquote><br />
</blockquote><a href="http://petrov.stanford.edu/pdfs/78.pdf" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img alt="image" border="0" class="left" height="120" src="http://petrov.stanford.edu/images/Lawrieetalthumbnail.jpg" width="90" /></a><b class="style1"></b><br />
One of the key insights from the neutral theory of molecular evolution is that functional sequences should generally evolve slower than nonfunctional sequences. The reasoning is very simple - some mutations in functional sequences will damage the function, will be removed by natural selection and thus will not contribute to evolutionary change. It is true that adaptation should speed up evolution because adaptive mutations would contribute to evolution at a much higher probability than neutral ones. This insight is the basis of much of comparative genomics. Find regions that evolve slower than neutral and you find functional sequences even if you know nothing about their function. Find paterns of evolution of functional regions that are too rapid and you find adaptation. Easy. In a <a href="http://petrov.stanford.edu/pdfs/78.pdf">paper published in GBE</a> by David Lawrie, Dmitri Petrov and Philipp Messer we show that this is not always so easy. Specifically, when mutation is strongly biased (say in favor of A and T nucleotides) and these nucleotides tend to be weakly deleterious, one can generate very fast flip-flopping between the mutationally preferred state (A and T) and selectively preferred state (G or C in this example). The rate of evolution might even exceed that expected under neutrality without any adaptation. We show that this effect might be important in comparative genomics and urge the development of comparative genomic methods that explicitly incorporate mutational biases, selective processes, and crucially their interactions. The paper has been evaluated by Faculty of 1000 (<a href="http://f1000.com/11045956">http://f1000.com/13188956</a> and here is <a href="http://petrov.stanford.edu/pdfs/Faster%20than%20neutral%20evolution%20of%20constrained%20sequences%3A%20the%20complex%20interplay%20of%20mutational%20biases%20and%20weak%20selection.%20-%20F1000.pdf">pdf</a>).Petrov Labhttp://www.blogger.com/profile/17303400627666039056noreply@blogger.com0tag:blogger.com,1999:blog-525744750539814123.post-29484453794905696942011-07-18T11:50:00.000-07:002011-12-26T11:53:19.458-08:00High rate of false positives in the estimates of positive selection due to faulty alignments<blockquote><br />
</blockquote><a href="http://petrov.stanford.edu/pdfs/77.pdf" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img alt="image" border="0" class="left" height="120" src="http://petrov.stanford.edu/images/PenkaGR2011.jpg" width="90" /></a><b class="style1"></b><br />
In a <a href="http://petrov.stanford.edu/pdf/77.pdf">paper published in Genome Research</a>, Penka Markova (who successfully graduated this year) and Dmitri, continue to shine light on the often underapprecaited step in studying natural selection in protein and DNA sequences. This step - alignment of homologous sequences - is key as it determines which positions in proteins are the "same" and thus can be meaningfully compared across species or individuals. Because it is often hard to assess the error at this step, the common practice is to accept the alignments as if they were in fact true and to investigate all other sources of possible error. Unfortunately, as this paper shows in particular, this assumption might be woefully wrong especially in the studies of positive selection. After all, we often define possible cases of positive selection by detecting patterns of evolution that are faster or different than predicted by the model of unchanging constraint. It is hard to generate a more unsual pattern than that produced by misalignments. Our paper suggests that 50-80% (!) of all cases of detected positive selection in the alighments of Drosophila proteins are due to misaligments. The problem is very severe and calls for computational and statistical solutions, manual curation of candidates, and above all caution in interpreting scans for positive selection based on massive, genome-level aligments of proteins. Our paper has been positively reviewed by Faculty of 1000 (two evaluations can be found here: <a href="http://f1000.com/11045956">http://f1000.com/11045956</a> and here is <a href="http://petrov.stanford.edu/pdfs/F1000%20evaluations%20of%20Markova%20and%20Petrov.pdf">pdf</a>).Petrov Labhttp://www.blogger.com/profile/17303400627666039056noreply@blogger.com0tag:blogger.com,1999:blog-525744750539814123.post-69691269913327755912011-04-23T11:51:00.000-07:002011-12-26T11:52:50.790-08:00Population Genomics of Transposable Elements in Drosophila<blockquote><br />
</blockquote><a href="http://petrov.stanford.edu/pdfs/76.pdf" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img alt="image" border="0" class="left" height="120" src="http://petrov.stanford.edu/images/F1.large.jpg" width="120" /></a><b class="style1"></b><br />
Transposable elements (TEs) are the primary contributors to the genome bulk in many organisms and are major players in genome evolution. TEs in <i>Drosophila melanogaster</i> come in a large diversity of families with individual familes varying in size from a few to over a hundred copies per genome.<a href="http://petrov.stanford.edu/pdfs/76.pdf"> In a paper that was just published in Molecular Biology and Evolution</a>, we carried out the first global population genomic analysis of ~800 TEs from all of the major families (55 in total) in 75 <i>D. melanogaster </i>strains. We found strong evidence that TEs in Drosophila are deleterious because ectopic recombination among dispersed TE copies generates inviable gametes. We showed that strength of this selection varies predictably with recombination rate, length of individual TEs, and copy number and length of other TEs in the same family. These rules do not appear to vary across orders, suggesting that selection based on ectopic recombination is a universal force preventing the uncontrolled spread of TEs in the Drosophila genome. Consistently with this notion we were able to build a statistical model that considered only individual TE-level (such as the TE length) and family-level properties (such as the copy number) and explained more than 40% of the variation in TE frequencies.Petrov Labhttp://www.blogger.com/profile/17303400627666039056noreply@blogger.com0tag:blogger.com,1999:blog-525744750539814123.post-64576213704852782652011-04-09T15:34:00.000-07:002012-01-02T15:35:53.074-08:00Ruth Hershberg accepts a tenure track faculty position offer from Technion<blockquote><br />
</blockquote><a href="http://petrov.stanford.edu/people.html#ruth" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img alt="image" border="0" class="left" height="156" src="http://petrov.stanford.edu/image/people/ruth.jpg" width="156" /></a><strong class="style1"></strong><br />
We are very happy to announce that <a href="http://petrov.stanford.edu/people.html#ruth">Ruth Hershberg</a> has just accepted a tenure track position at the <a href="http://md.technion.ac.il/">Ruth & Bruce Rappaport Faculty of Medicine</a> at the <a href="http://www1.technion.ac.il/en">Technion</a> (Israel Institute of Technology). Ruth will establish an interdisciplinary lab, combining evolutionary theory, bioinformatics, computational and experimental genomics, and microbiology. She will continue studying the most fundamental driving forces in evolution: mutation and natural selection, and elucidating how each of these process shapes microbial genomic variation. More specifically Ruth will pursue the following topics: (i) Elucidating variation in the efficacy with which natural selection acts on different bacteria, and understanding the consequences of such variation on the evolution of bacterial genomes, (ii) Studying variation in mutational patterns across bacteria, (iii) Quantifying changes in mutational rates and patterns in response to stress, (iv) Understanding the evolutionary processes that drive codon usage bias, (v) The bacterial species concept.<br />
The <a href="http://www1.technion.ac.il/en">Technion</a> is one of Israel’s top Universities, and provides some of the best research resources available in Israel. Ruth has been a star in the lab, publishing several beautiful papers, showing: (i) <a href="http://petrov.stanford.edu/publications.html#65"> how the identity of optimal codons is chosen in evolution</a>, (ii) <a href="http://petrov.stanford.edu/publications.html#592"> that mutation is universally biased towards AT in bacteria and that variable genomic GC content is likely driven by natural selection</a>, (iii) <a href="http://petrov.stanford.edu/publications.html#56"> that the reduced selection on M. tuberculosis leads to high functional diversity</a>, and (iv) <a href="http://petrov.stanford.edu/publications.html#49">that the reduced selection on Shigella led to a loss of many genes</a>. We will miss her very much and hope to collaborate with her in the future. <strong><a href="mailto:rutihersh@gmail.com">Anyone interested in joining Ruth’s lab, as either a postdoc, graduate or undergraduate student, or in collaborating with Ruth in any other way should contact her at rutihersh@gmail.com. </a></strong>Petrov Labhttp://www.blogger.com/profile/17303400627666039056noreply@blogger.com0tag:blogger.com,1999:blog-525744750539814123.post-26819834749371161532011-03-26T13:00:00.000-07:002011-03-26T17:54:48.593-07:00T-lex: automatic assessment of the presence of individual transposable elements using next generation sequence data<a href="http://petrov.stanford.edu/pdfs/77.pdf" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img alt="image" border="0" class="left" height="120" src="http://petrov.stanford.edu/images/Tlex.jpg" width="120" /></a><br />
<a href="http://petrov.stanford.edu/people.html#anna">Anna-Sophie Fiston-Lavier</a> and <a href="http://petrov.stanford.edu/people.html#josefa">Josefa González</a> (with the participation of a summer student Matthew Carrigan and <a href="http://petrov.stanford.edu/people.html#dmitri">Dmitri)</a> have just published a very powerful and easy to use tool for the assessment of presence/absence of known TEs in the new resequenced genomes. The <a href="http://nar.oxfordjournals.org/cgi/content/abstract/39/6/e36?ct=ct">paper</a> was published in Nucleic Acids Research (with the open access option) and we hope that people will find it helpful. This tool, which we called <strong>T-lex</strong> (<strong>T</strong> for transposable element and <strong>-lex</strong> for Solexa), obviates the need to run thousands of PCR in order to study population genetics of TEs and, more specifically for us, to find <a href="http://petrov.stanford.edu/newstext.html#TEadaptation">TEs that are likely to be adaptive</a>. Anna-Sophie is working now on a new module for this program that would also allow us to detect new TE insertions in the nextgen data. Together these two programs (in conjunction with several other similar programs that are becoming available now) will revolutionize the TE research for us. To read more about T-lex or to use it please go to http://petrov.stanford.edu/cgi-bin/Tlex_manual.html. <strong>Note that you can run T-lex (or other scripts) on a cloud using the <a href="http://www.scalegenomics.com/">Scalegenomics.com</a></strong> <strong>next-generation cloud service. <a href="http://scalegenomics.com/"> </a></strong> We are in the process of creating the T-lex ScaleGenomics app so that you can run T-lex without any installation hassles.<br />
<br />
<strong>Please give us feedback about T-lex by leaving comments here!</strong>Petrov Labhttp://www.blogger.com/profile/17303400627666039056noreply@blogger.com0tag:blogger.com,1999:blog-525744750539814123.post-14967768078813464742011-02-25T16:30:00.000-08:002011-02-25T16:30:33.734-08:00Alan Bergland wins prestigious NIH postdoctoral fellowship<a href="http://www.stanford.edu/%7Ebergland" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img alt="image" border="0" class="left" height="122" src="http://petrov.stanford.edu/image/alansmall.jpg" width="120" /></a><strong class="style1"><a class="style2" href="http://www.stanford.edu/%7Ebergland">Alan Bergland wins prestigious NIH postdoctoral fellowship</a></strong><br />
<a href="http://www.stanford.edu/%7Ebergland">Alan Bergland</a> was just awarded an NIH NRSA postdoctoral fellowship to study the evolution of <em>Drosophila melanogaster</em> in temperate climates. The experiments outlined in his proposal will use whole genome resequencing of populations of flies collected along latitudinal clines and through the growing season. These data will allow him to test hypotheses about the demographic consequences of seasonal population booms and busts. He will also be able to use these data to identify alleles that show both latitudinal and seasonal variation; these spatially and temporally balanced polymorphisms are likely to directly underlie adaptation to temperate environments. <br />
This fellowship will give Alan the opportunity to learn population genomics and will complement his graduate studies on evolutionary quantitative genetics of life history traits. The project is going to be done in collaboration with Prof. Paul Schmidt (U. Penn) - the premier scholar in Drosophila evolutionary biology and genetics of adaptation to temperate climates.Petrov Labhttp://www.blogger.com/profile/17303400627666039056noreply@blogger.com0tag:blogger.com,1999:blog-525744750539814123.post-84825039718823187502010-12-07T13:57:00.001-08:002010-12-07T13:57:36.956-08:003rd Semiannual Bay Area Population Genomics Conference<strong class="style1"><a class="style2" href="http://www.stanford.edu/group/petrov/BAPG.html"><img align="left" height="200" src="http://petrov.stanford.edu/images/images-1.jpg" width="150" /></a></strong><strong class="style1"></strong><br />
The schedule for <a href="http://www.stanford.edu/group/petrov/BAPG.html">BAPG III</a> at Stanford is all set. This time and hopefully in the future BAPG is sponsored by the <a href="http://www.stanford.edu/group/ecoevo">Ecology and Evolution Group</a> at the <a href="http://biology.stanford.edu/index.php">Stanford Biology Department</a>. We have an exceptional lineup of speakers from Berkeley, UC Santa Cruz and Stanford. The meeting will start at 9AM with coffee and will end with lunch and a poster session.<br />
<strong>9:30 AM Rachel Brem, UC Berkeley </strong><br />
Pathway evolution in Saccharomyces <br />
<strong>10:00 AM Dario Valenzano, Stanford </strong><br />
Genetic Architecture of longevity in the short-lived fish <br />
Nothobranchius furzeri <br />
<strong>10:30 AM Paul Jenkins, UC Berkeley </strong><br />
A new approach to computing likelihoods in population genetics models <br />
with recombination <br />
<strong>11:30 AM Jared Wenger, Stanford </strong><br />
Adaptive mutations effect minimal trade-offs across the yeast adaptive <br />
landscape <br />
<strong>12:00 PM Ed Green, UC Santa Cruz </strong><br />
Recent human evolution as revealed by ancient hominin genome <br />
sequences<br />
<br />
For additional information (schedule, parking, registration, poster lineup), the latest news and the videos of the presentation after the conference please go to<br />
<a href="http://www.google.com/url?sa=D&q=http://www.stanford.edu/group/petrov/BAPG.html&usg=AFQjCNE1N7a3SKUEbMvW6z6GuW4S23SG0g">http://www.stanford.edu/group/petrov/BAPG.html</a>Petrov Labhttp://www.blogger.com/profile/17303400627666039056noreply@blogger.com0tag:blogger.com,1999:blog-525744750539814123.post-46411371566615627492010-12-04T12:41:00.000-08:002010-12-04T13:11:27.241-08:00Broker Genes in Human Disease<b class="style1"><a class="style2" href="http://petrov.stanford.edu/pdfs/74.pdf"><img align="left" height="170" src="http://petrov.stanford.edu/images/protein_network.jpg" width="150" /></a></b><b class="style1"><a class="style2" href="http://petrov.stanford.edu/pdfs/74.pdf"> </a></b><br />
Genes that underlie human disease are important subjects of systems biology research. <a href="http://petrov.stanford.edu/pdfs/74.pdf">In a paper just published in GBE</a> by <a href="http://people.tamu.edu/%7Ejcai/">James Cai</a>, <a href="http://elbo.gs.washington.edu/">Elhanan Borenstein</a> and <a href="http://petrov.stanford.edu/people.html#dmitri">Dmitri</a>, we demonstrated that Mendelian and complex disease genes have distinct and consistent protein–protein interaction (PPI) properties. Disease genes have unusually high degree (number of connections to other proteins) and low clustering coefficients (their neighbor proteins tend not to be connected). <strong>We describe such genes as brokers in that they connect many proteins that would not be connected otherwise.</strong> In contrast, disease genes identified in genome-wide association study (GWAS) do not have these broker properties. We suggest that the mapping of the GWAS-identified SNPs onto the genes underlying disease is highly error prone. This research can be used to help improve this mapping and prioritize the identification of disease genes in GWAS studies.Petrov Labhttp://www.blogger.com/profile/17303400627666039056noreply@blogger.com0tag:blogger.com,1999:blog-525744750539814123.post-22733024004040659172010-10-02T15:01:00.000-07:002010-10-10T19:09:02.320-07:00Universal patterns of mutation<div class="separator" style="clear: both; font-family: Arial,Helvetica,sans-serif; text-align: center;"></div><div class="separator" style="clear: both; font-family: Arial,Helvetica,sans-serif; text-align: center;"><span style="font-size: small;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjQO80Spas9OYxcHar9KuIu5hVrkilyksZOvO-dV5Sz84n9l5kuWDaKX099WChjgyLoc-TVvdXIlnPAJrOO8vk8awHGYSzjKLszvilgb5DrHXnIRtymVaJr48lOZ1lX4r12ELh8nIyP4mwE/s1600/Phylogeny.jpg" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" height="200" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjQO80Spas9OYxcHar9KuIu5hVrkilyksZOvO-dV5Sz84n9l5kuWDaKX099WChjgyLoc-TVvdXIlnPAJrOO8vk8awHGYSzjKLszvilgb5DrHXnIRtymVaJr48lOZ1lX4r12ELh8nIyP4mwE/s200/Phylogeny.jpg" width="150" /></a></span></div><div style="font-family: Arial,Helvetica,sans-serif;"><span style="font-size: small;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjoODyEig3v3JK4dEjSjvmSdYCCyO9i4BGtkFfusfuMa_ZLFYlZsrxonWoW5WuHoKXmOPRnvueayASXW4c-FsRjD0hhZXo3fplJ6O-Y0JOr47oTE6vhb2MDhSoWlKwvK8WjmsSJ_EUq77XX/s1600/Phylogeny.jpg" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><br />
</a></span></div>Natural selection sorts through the variability generated by mutation and biases evolution toward fitter outcomes. Mutation, while generally agnostic to fitness can also bias evolutionary outcomes because certain types of mutations occur more frequently than others. For instance, it was generally assumed that the extreme variation observed in nucleotide content among bacteria (from ~20% to ~80% GC) is predominantly driven by extreme differences in mutational biases between different bacterial lineages. Under such an assumption, mutation would have to be strongly AT-biased in some lineages and strongly GC-biased in others. In sexually reproducing organisms mutational biases can be investigated by examining low frequency polymorphisms. In bacteria, however, this has not been possible because the concepts of species and polymorphism are ill-defined. <a href="http://www.plosgenetics.org/article/info%3Adoi/10.1371/journal.pgen.1001115">In a paper recently published in PLoS Genetics</a>, <a href="http://petrov.stanford.edu/people.html#ruth">Ruth Hershberg</a> and <a href="http://petrov.stanford.edu/people.html#dmitri">Dmitri Petrov</a> demonstrated that bacterial lineages that recently developed clonal, pathogenic lifestyles evolve under extremely relaxed selection, and are uniquely suitable for the study of bacterial mutational biases. We analyzed large sequence datasets from five clonal pathogens in four diverse bacterial clades spanning most of the range of genomic nucleotide content. Contrary to expectations they found that mutation is AT-biased in every case to a very similar degree. Furthermore in each case mutation is dominated by transitions from C/G to T/A. These findings demonstrate that mutational biases are far les variable than previously assumed and that variation in bacterial nucleotide content is not due entirely to mutational biases. Rather natural selection or a selection like process such as biased gene conversion must strongly affect nucleotide content in bacteria. A paper by Hildebrand and colleagues published back-to-back to ours inthe same issue of PLoS Genetics reached similar conclusions: <a href="http://petrov.stanford.edu/pdfs/journal.pgen.1001107.pdf">Evidence of Selection upon Genomic GC-Content in Bacteria</a>. PLoS Genetics also published a commentary on this work by Eduardo Rocha and Edward Feil: <a href="http://petrov.stanford.edu/pdfs/journal.pgen.1001104.pdf">Mutational Patterns Cannot Explain Genome Composition: Are There Any Neutral Sites in the Genomes of Bacteria?</a>Petrov Labhttp://www.blogger.com/profile/17303400627666039056noreply@blogger.com0tag:blogger.com,1999:blog-525744750539814123.post-24363868133941046312010-08-19T14:19:00.000-07:002010-08-20T15:46:48.379-07:00Physics of Evolution<a href="http://ctbp.ucsd.edu/workshops/index.php?id=29" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img alt="image" border="0" class="left" height="119" src="http://petrov.stanford.edu/images/wolynes.jpg" width="144" /></a><br />
Dmitri is going to present two lectures at the <a href="http://ctbp.ucsd.edu/workshops/index.php?id=29">"Physics of Evolution" workshop</a> at UC San Diego at the end of this month. The workshop is dedicated to the applications of statistical physics to quantification of evolutionary process. The organizers say that:"This summer school will introduce graduate students and postdoctoral researchers in the fields of biological physics, statistical mechanics and non-equilibrium processes to the opportunities and challenges present in the area of Darwinian evolutionary dynamics. These have been enabled by sequencing technology advances, a new generation of quantitative laboratory-scale experiments, and new concepts in theoretical approaches to complex systems. Topics to be covered include: modern genomics tools, microorganism experiments, mutation-selection theory, the role of recombination and horizontal gene transfer, and applications to both the immune system and to infectious disease". Dmitri will talk about two papers: (1) one about our recent finding that Drosophila appears to have such <a href="http://petrovlabblog.blogspot.com/2010/07/tuesday-july-13-2010-every-mutation-at.html">large effective population sizes</a> that adaptation is not limited by mutation and (ii) one on the recent work of a postdoc in the lab, <a href="http://petrov.stanford.edu/people.html#ruth">Ruth Hershberg</a>,that mutation appears to be always biased towrads A's and T's across all bacteria potentially implying that GC-rich bacterial genomes are under selection to be GC rich. The paper about Ruth's work is about to come out in PloS Genetics.Petrov Labhttp://www.blogger.com/profile/17303400627666039056noreply@blogger.com0tag:blogger.com,1999:blog-525744750539814123.post-49250198993882830592010-07-29T17:57:00.000-07:002010-07-30T12:09:25.450-07:00James Cai is a new Assistant Professor at Texas A&M!<div class="separator" style="clear: both; text-align: center;"><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjtxh8oTduEkp2VVn16j8AI8dsOky6EnKKzNc-API3LfK77iQgXnTfMDlKGyN4Qjq8-X98zKscaBOlAzHNSxPMNzsjnimJWy-x0HMWIfO4HQ3jHJ7w6MrDiZGpd-VET8HptsrxfystXNkwG/s1600/James+Viola.JPG" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjtxh8oTduEkp2VVn16j8AI8dsOky6EnKKzNc-API3LfK77iQgXnTfMDlKGyN4Qjq8-X98zKscaBOlAzHNSxPMNzsjnimJWy-x0HMWIfO4HQ3jHJ7w6MrDiZGpd-VET8HptsrxfystXNkwG/s320/James+Viola.JPG" /></a></div>We are very happy to announce that <a href="http://petrov.stanford.edu/people.html#james">James Cai</a>, a postdoctoral fellow in the lab, has accepted an offer for a tenure-track Assistant Professor position at Texas A&M University, Department of Veterinary Integrative Biosciences. He will be moving in September and is already starting to build a computational genomics laboratory there. (<a href="http://www.genomezoo.net/home/postdoctoralpositionincomputationalevolutionarygenomics">See the ad for a postdoctoral position in James's new lab</a>.) His group will focus on computational research in population genomics and molecular evolution, applying population genetic theory to modern biological data and developing statistical tests and computational tools to investigate evolutionary processes shaping genome variability patterns within and between species. <a href="http://petrov.stanford.edu/people.html#james">James</a> joined our lab in 2006 after the completion of his Ph.D. at the University of Hong Kong. Viola Luo, James's wife pictured above, moved from Hong Kong to the Bay Area and joined James at Stanford in 2007, where she started her career in regulatory affairs of clinical trials at Stanford Cancer Center. In our lab, James focused on understanding how positive selection shapes patterns of polymorphism in the human genome and published a <a href="http://petrov.stanford.edu/pdfs/58.pdf">key paper</a> that showed for the first time that positive selection is indeed pervasive in the human genome and does leave the expected signatures in the patterns of polymorphism. See the description of this research in <a href="http://news.stanford.edu/news/2009/january21/evoladap-012109.html">Stanford Daily</a>. James was also interested how the timing of the gene's entry into the genome (gene age) interacts with the gene's importance to the functioning of the organism and the way natural selection shapes its evolution. <a href="http://petrov.stanford.edu/publications">He published a series of papers on this topic as well</a>. Finally, James is famous for creating a set of Matlab based toolkits for <a href="http://bioinformatics.org/pgetoolbox">population genetics</a> and <a href="http://bioinformatics.org/mbetoolbox">molecular evolution</a>. We are all extremely proud of James and wish him the best of luck in his brilliant young career!Petrov Labhttp://www.blogger.com/profile/17303400627666039056noreply@blogger.com1tag:blogger.com,1999:blog-525744750539814123.post-63734703362467733642010-07-13T11:36:00.000-07:002010-07-30T11:50:21.524-07:00Every mutation, at every site, at any given time<a href="http://www.plosgenetics.org/article/info%3Adoi/10.1371/journal.pgen.1000924" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img alt="image" border="0" class="left" height="150" src="http://petrov.stanford.edu/images/journal.pgen.1000987.g001.png" width="120" /></a>Adaptation in eukaryotes is often assumed to be limited by the waiting time for adaptive mutations. This is because effective population sizes are believed to be relatively small, typically on the order of only a few million reproducing individuals or less. It should therefore take hundreds or even thousands of generations until a particular new mutation emerges. However, several striking examples of rapid adaptation appear inconsistent with this view. In a paper just published by <a href="http://www.plosgenetics.org/article/info%3Adoi/10.1371/journal.pgen.1000924">PloS Genetics,</a> we (co-first authors <a href="http://petrov.stanford.edu/people2.html#talia">Talia Karasov</a> and <a href="http://petrov.stanford.edu/people.html#philipp">Philipp Messer</a>, and <a href="http://petrov.stanford.edu/people.html#dmitri">Dmitri</a>) investigate a showpiece case for rapid adaptation, the evolution of pesticide resistance in the classical genetic organism <i>Drosophila melanogaster</i>. Our analysis reveals distinct population genetic signatures of this adaptation that can only be explained if the number of reproducing flies is, in fact, more than 100-fold larger than commonly believed. We argue that the old estimates, based on standing levels of neutral genetic variation, are misleading in the case of rapid adaptation because levels of standing variation are strongly affected by infrequent population crashes or adaptations taking place in the vicinity of neutral sites. <b>We suggest that much of the time adaptation in Drosophila takes place in populations that are much larger that a billion meaning that every single-step mutation at every site exists in the population at every given time.</b> This means that soft sweeps should be very common and that complex, multi-step adaptations should fix all at once without intermediate fixations of single-step mutations. We also argue that adaptation should be not mutation-limited in all species with population sizes that exceed a billion (roughly the inverse of mutation rate per site), which is the case for many insects and most marine invertebrates. Nick Barton wrote a <a href="http://www.plosgenetics.org/article/info%3Adoi%2F10.1371%2Fjournal.pgen.1000987">great perspective article</a> and the work was also highlighted in <a href="http://www.nature.com/nrg/journal/vaop/ncurrent/full/nrg2838.html">Nature Review Genetics</a> and <a href="http://petrov.stanford.edu/pdfs/Scannel&EisenF1000article.pdf">Faculty of 1000</a>. It is currently in the top 10 most viewed articles on <a href="http://f1000biology.com/top10/mostviewed/">Faculty of 1000</a> and in PLoS Genetics.Petrov Labhttp://www.blogger.com/profile/17303400627666039056noreply@blogger.com0tag:blogger.com,1999:blog-525744750539814123.post-68906239927759080902010-04-25T11:42:00.000-07:002010-07-30T11:49:52.274-07:00Nadia Singh is the newest Assistant Professor in the Genetics Department at NC State<a href="http://cals.ncsu.edu/genetics/index.php/people/nadia-singh" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img alt="image" border="0" class="left" height="150" src="http://petrov.stanford.edu/images/NDS.jpg" width="120" /></a><br />
<a href="http://petrov.stanford.edu/people2.html#nadia">Nadia Singh</a>, a former PhD student in the lab, has accepted an Assistant Professor position in the <a href="http://cals.ncsu.edu/genetics/">Genetics Department at the North Carolina State University</a>. Nadia received her PhD from Stanford in 2006, and went on to a postdoctoral position at Cornell University in the labs of <a href="http://mbg.cornell.edu/cals/mbg/research/clark-lab/current_members.cfm">Andy Clark</a> and <a href="http://mbg.cornell.edu/cals/mbg/research/aquadro-lab/currentmembers.cfm">Chip Aquadro</a>. Nadia will begin her new position at NCSU in the Fall of 2010. NCSU has a wonderfully rich community with a strong emphasis on molecular, quantitative, developmental, computational, and statistical genetics, and Nadia is looking forward to continuing her work on mutation and recombination rate variation in Drosophila in this new and interactive environment. Nadia is the first lab graduate student to start her own lab. We are all extremely proud and wish Nadia the best of luck!Petrov Labhttp://www.blogger.com/profile/17303400627666039056noreply@blogger.com0tag:blogger.com,1999:blog-525744750539814123.post-14378625033368575732010-04-09T11:46:00.000-07:002010-07-30T11:50:08.127-07:00Adaptation to temperate climates in Drosophila<a href="http://petrov.stanford.edu/pdfs/69.pdf" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img alt="image" border="0" class="left" height="129" src="http://petrov.stanford.edu/images/journal.pgen.1000905.g001.png" width="120" /></a><br />
The potential of geographic studies of genetic variation for the understanding of adaptation has been recognized for some time. In Drosophila, most of the available studies are based on <i>a priori</i> candidates giving a biased picture of the genes and traits under spatially varying selection. <a href="http://petrov.stanford.edu/pdfs/69.pdf">In a paper just published in PLoS Genetics</a> and led by <a href="http://petrov.stanford.edu/people.html#josefa">Josefa Gonzalez</a>, we performed a genome-wide scan of adaptations to temperate climates associated with Transposable Element (TE) insertions. We integrated the available information of the identified TEs and their nearby genes to provide plausible hypotheses about the phenotypic consequences of these insertions. Considering the diversity of these TEs and the variety of genes into which they are inserted, it is surprising that their adaptive effects are consistently related to temperate climate-related factors. The TEs identified in this work add substantially to the markers available to monitor the impact of climate change on populations.Petrov Labhttp://www.blogger.com/profile/17303400627666039056noreply@blogger.com0tag:blogger.com,1999:blog-525744750539814123.post-88001973427223799242010-03-01T11:51:00.000-08:002010-07-30T11:51:46.906-07:00Philip Bulterys is accepted to UCLA MD/PhD program!<a href="http://petrov.stanford.edu/people.html#philip" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img alt="image" border="0" class="left" height="177" src="http://petrov.stanford.edu/image/people/philiplabphoto.jpg" width="120" /></a><strong class="style1"></strong><br />
<a href="http://petrov.stanford.edu/people.html#philip">Philip Bulterys</a>, a fourth-year undergraduate in the lab, was just accepted into the extremely prestigious <a href="http://mstp.healthsciences.ucla.edu/pages/">UCLA MD/PhD program (MSTP)</a>. Philip grew up in pre-genocide Rwanda and attended high school in Lusaka, Zambia. His parents are both medical epidemiologists and Philip became interested in public health at an early age. As a high school student he volunteered in the malnutrition ward of the University Teaching Hospital, initiated a street-kids project with friends, and conducted a microbial water quality study to look for fecal coliforms in a local community’s drinking water. He has also participated in the emergency response to the HIV epidemic - the response partly led by Philip's parents. He is firmly and passionately committed to public health and understanding, preventing, and curing infectious disease. Philip is currently working on an HIV evolution project and hopes to continue studying the evolution and transmission of infectious diseases throughout his training and career. We are all extremely proud and extend our congratulations for an honor and an opportunity that is so richly deserved.Petrov Labhttp://www.blogger.com/profile/17303400627666039056noreply@blogger.com0tag:blogger.com,1999:blog-525744750539814123.post-90658805608273352412010-02-17T12:08:00.000-08:002010-07-30T12:08:44.478-07:00Fabian Staubach is joining our lab in May 2010!<a href="http://petrov.stanford.edu/people.html#fabian" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img alt="image" border="0" class="left" height="150" src="http://petrov.stanford.edu/image/fabiansmall.jpg" width="120" /></a><strong class="style1"><a class="style2" href="http://petrov.stanford.edu/people.html#fabian"></a></strong><br />
<a href="http://petrov.stanford.edu/people.html#fabian">Fabian Staubach</a> from the Max Planck Institute for Evolutionary Biology is joining our lab in May 2010! During his Ph.D. research he worked on the evolution of gene expression in natural populations of house mice (<em>Mus musculus</em>) and found a <em>de novo</em> originated gene in the mouse lineage. Currently he is finishing his work on a 600k mouse genotyping array applied to natural populations and a metagenomics 454 sequencing project on the gut flora of mice. For his research he applied and developed a variety of molecular biology, statistical, and bioinformatics tools to shed light on transcriptional evolution, mouse population genetics and the evolution of new genes. Fabian will work on natural selection and adaptation in <em>Drosophila</em>.<br />
For more information please go to: http://www.evolbio.mpg.de/english/people/staff/wissPersonal/wissM19/index.htmlPetrov Labhttp://www.blogger.com/profile/17303400627666039056noreply@blogger.com0tag:blogger.com,1999:blog-525744750539814123.post-320047456606612842010-02-01T12:10:00.000-08:002010-07-30T12:11:54.585-07:00Second Bay Area Population Genomics Conference<a href="http://groups.google.com/group/bayareapopulationgenomics" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img alt="image" border="0" class="left" height="90" src="http://petrov.stanford.edu/images/BayArea.jpg" width="90" /></a><b class="style1"></b><br />
On the heels of the success of the first Bay Area Population Genomics Conference at Stanford in the Fall 0f 2009 we are planning the second BAPG Conference at Berkeley on March the 13th. The labs of Doris Bachtrog, Michael Eisen, and Rasmus Nielsen are going to take the lead in organizing. Students and faculty from Stanford, Berkeley, UCSF, and UC Davis will be represented.<br />
<br />
If you want to receive updated news about the BAPG conference please join<br />
<a href="http://groups.google.com/group/bayareapopulationgenomics"><b>http://groups.google.com/group/bayareapopulationgenomics</b></a><br />
<br />
The PI's should also join: <a href="http://groups.google.com/group/bay-area-population-genetics/"><b>http://groups.google.com/group/bay-area-population-genetics/</b></a>Petrov Labhttp://www.blogger.com/profile/17303400627666039056noreply@blogger.com0tag:blogger.com,1999:blog-525744750539814123.post-70812325290160067452010-01-13T12:12:00.000-08:002010-07-30T12:12:55.834-07:00Alan Bergland is joining the lab<a href="http://petrov.stanford.edu/people.html#alan" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img alt="image" border="0" class="left" height="122" src="http://petrov.stanford.edu/image/alansmall.jpg" width="120" /></a><strong class="style1"><a class="style2" href="http://petrov.stanford.edu/people.html#alan"></a></strong><br />
We are excited that Alan Bergland from Brown University has decided to join our lab! Alan is currently finishing up his Ph.D. research (<a href="http://www.brown.edu/Departments/EEB">http://www.brown.edu/Departments/EEB</a>) which focused on understanding the interplay between environmental variation and both long- and short-term evolutionary processes. Specifically he studied the relationship between larval nutrition and adult fecundity in <i>Drosophila melanogaster</i>. This research used an impressive array of tools and concepts from evolutionary demography, ecology, molecular and quantitative genetics, and physiology to investigate how life history plasticity evolves in natural populations. Alan will arrive in September 2010 and will focus on the population and molecular genetics of local adaptation in <i>Drosophila</i>.Petrov Labhttp://www.blogger.com/profile/17303400627666039056noreply@blogger.com0tag:blogger.com,1999:blog-525744750539814123.post-10028121708475445992009-10-26T12:13:00.000-07:002010-07-30T19:02:44.783-07:00First Bay Area Population Genomics Conference<a href="http://groups.google.com/group/bayareapopulationgenomics" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img alt="image" border="0" class="left" height="90" src="http://petrov.stanford.edu/images/BayArea.jpg" width="90" /></a><b class="style1"><a class="style2" href="http://groups.google.com/group/bayareapopulationgenomics"> </a></b><br />
We just hosted the first Bay Area Population Genomics Conference at Stanford. Students and faculty from Stanford, Berkeley, UCSF, and UC Davis were represented. We met at 9AM for breakfast, heard 5 great <a href="http://petrov.stanford.edu/pdfs/AbstractsBAPGC-10_22_09.pdf">talks</a> from 10AM to 2PM, had lunch and talked about posters. The turnout, the talks, and the conversations were great. By all accounts it was a great success. We hope to have BAPG conferences take place every quarter. The next BAPG conference is likely to take place at Berkeley in the Winter Quarter with Michael Eisen and Rasmus Nielsen's groups taking the lead in organizing it.<br />
<br />
If you want to receive news about the BAPG conference please join <a href="http://groups.google.com/group/bayareapopulationgenomics">http://groups.google.com/group/bayareapopulationgenomics</a><br />
<br />
<a href="http://petrov.stanford.edu/pdfs/AbstractsBAPGC-10_22_09.pdf">Talks</a>: <b>Graham Coop</b>, UC Davis, Graham Coop Lab, "<b>Meiotic<br />
recombination hotspots in humans and mice</b>"<br />
<br />
<b>Dan Kvitek</b>, Stanford, Gavin Sherlock Lab, "<b>Molecular<br />
characterization of the fitness landscape in asexually evolving<br />
populations of Saccharomyces cerevisiae</b>"<br />
<br />
<b>David Goode</b>, Stanford, Arend Sidow Lab, "<b>Evolutionary<br />
constraint facilitates interpretation of genetic variation in<br />
resequenced human genomes</b>"<br />
<br />
<b>Qi Zhou</b>, Berkeley, Doris Bachtrog Lab, "<b>Deciphering neo-sex<br />
and B chromosome evolution by the complete genome of Drosophila<br />
albomicans</b>"<br />
<br />
<b>Hunter Fraser</b>, Stanford, Hunter Fraser Lab,<br />
"<b>Widespread adaptive evolution of gene expression in budding yeast</b>"Petrov Labhttp://www.blogger.com/profile/17303400627666039056noreply@blogger.com0tag:blogger.com,1999:blog-525744750539814123.post-85742482278897109322009-10-07T16:13:00.000-07:002010-07-30T19:01:52.754-07:00"Great fleas have little fleas upon their backs to bite 'em, and little fleas have lesser fleas, and so ad infinitum"<div style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img alt="image" border="0" class="left" height="120" src="http://petrov.stanford.edu/image/325_1352_F1.gif" width="120" /><b class="style1"></b></div>Transposable Elements (TEs) are fragments of DNA that can jump from one genome position to another producing extra copies of themselves in the process. In a recent issue of Science, <a href="http://petrov.stanford.edu/people.html#josefa">Josefa Gonzalez</a> and <a href="http://petrov.stanford.edu/people.html#dmitri">Dmitri Petrov</a> write a <a href="http://petrov.stanford.edu/pdfs/66.pdf">perspective</a> on a <a href="http://petrov.stanford.edu/pdfs/Tuned-for-transposition.pdf">paper by Yang et al</a> which showed how some TEs manage to dispense with almost all of their sequences and still remain extremely prolific. TEs generally encode among other genes proteins that promote their mobility, either a reverse transcriptase or a transposase and parasitize the key cellular functions. Interestingly, such TEs are themselves often parasitized. These parasites of parasites -- less judgmentally called non-autonomous TEs -- contain key recognition sequence required for mobility but dispense with making the protein products required for transposition. A spectacularly successful type of non-autonomous TEs, called MITEs, has been discovered fairly recently in plants. MITEs are present in many thousand copies in many plant genomes but because they are so small (~100- 500 bp) and encode no proteins it was hard to understand how they move. We now have a very good model but still have plenty of unresolved puzzles. For more details read our <a href="http://petrov.stanford.edu/pdfs/66.pdf">Perspective</a> and the <a href="http://petrov.stanford.edu/pdfs/Tuned-for-transposition.pdf">Yang et al. paper</a>.Petrov Labhttp://www.blogger.com/profile/17303400627666039056noreply@blogger.com0tag:blogger.com,1999:blog-525744750539814123.post-40111121333818537612009-10-07T12:18:00.000-07:002010-07-30T12:19:14.184-07:00Graduate School Applications are due December 1, 2009<a href="http://petrov.stanford.edu/join.html" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img alt="image" border="0" class="left" height="120" src="http://petrov.stanford.edu/images/DSCN5461.jpg" width="120" /></a><strong class="style1"></strong><br />
If you are intetested in joining our lab as a graduate student, the deadline for applications is December 1. The <a href="http://biosciences.stanford.edu/admissions.html">Graduate Bioscience Admissions</a> program coordinates all graduate admissions in the biological sciences at Stanford. Please consult their website for the current application procedures. Don't be scared off by the fact that the site is located in the medical school domain. It is this way for bureaucratic reasons only. It is essential that you list <a href="http://petrov.stanford.edu/people.html#dmitri">Dmitri</a> as a potential advisor on your application form if you are interested in joining our lab and also to mark the <strong>Department of Biology</strong> and choose <strong>"evolution and ecology"</strong> as your interest within that. This will ensure that Dmitri will see your application. Also contact Dmitri ahead of time (<a href="mailto:dpetrov@stanford.edu">dpetrov@stanford.edu</a>) - and he will also help you with the admissions process. In general, it is a realy good idea to contact your potential advisors if you want to be successful in the admissions process. Departmental funding for graduate study at Stanford is limited. It is important to apply for an NSF Graduate Fellowship and any other sources of external funding at the same time as you are applying for graduate study.Petrov Labhttp://www.blogger.com/profile/17303400627666039056noreply@blogger.com0tag:blogger.com,1999:blog-525744750539814123.post-16945921215849651342009-08-21T16:15:00.000-07:002010-07-30T16:16:13.704-07:00Papers from the lab are getting noticed<div style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img alt="image" border="0" class="left" height="90" src="http://petrov.stanford.edu/images/DSCN5461.jpg" width="120" /><strong class="style1"><a class="style2" href="http://petrov.stanford.edu/people.html#yuan"></a></strong></div><br />
First, <a href="http://petrov.stanford.edu/pdfs/RutiNatureReviewsGenetics.pdf">Nature Review Genetics</a> highlighted <a href="http://petrov.stanford.edu/people.html#ruth">Ruth Hershberg's </a><a href="http://petrov.stanford.edu/pdfs/65.pdf">PLoS Genetics paper</a>. And then Genetics published a <a href="http://petrov.stanford.edu/pdfs/63.pdf">paper</a> by <a href="http://petrov.stanford.edu/people.html#philipp">Philipp Messer</a> and highlighted it on the <a href="http://petrov.stanford.edu/pdfs/GeneticsCoverPhilipp.pdf">cover</a> and in the <a href="http://www.genetics.org/cgi/content/full/182/4/NP">highlights</a>. Yay for us! More details about Philipp's paper to follow.Petrov Labhttp://www.blogger.com/profile/17303400627666039056noreply@blogger.com0tag:blogger.com,1999:blog-525744750539814123.post-60663309295062877952009-08-21T16:14:00.000-07:002010-07-30T19:02:28.254-07:00Estimating mutational rates and patterns from new genomic data<div style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img alt="image" border="0" class="left" height="120" src="http://petrov.stanford.edu/images/fig_web.jpg" width="120" /><b class="style1"></b></div>Mutations are the foundation of genetic diversity, yet we remain uncertain about their rates and patterns. This is because new mutations are difficult to assess experimentally as they occur at extremely low rates in individuals. Indirect estimates of mutation rates from levels of divergence or heterozygosity suffer from unknown selective and demographic biases and disregard deleterious mutations. In a <a href="http://petrov.stanford.edu/pdfs/63.pdf">paper</a> just published by Genetics <a href="http://petrov.stanford.edu/people.html#philipp">Philipp Messer</a> demonstrates how unbiased mutation rate estimates can be obtained from polymorphism data gathered from deep sequencing projects. This promises to facilitate the assessment of several long-standing problems of evolutionary biology. The paper is also featured in the issue <a href="http://www.genetics.org/cgi/content/full/182/4/NP">highlights</a> and on the <a href="http://petrov.stanford.edu/pdfs/GeneticsCoverPhilipp.pdf">cover of Genetics' August issue</a>.Petrov Labhttp://www.blogger.com/profile/17303400627666039056noreply@blogger.com0tag:blogger.com,1999:blog-525744750539814123.post-32148120511922061962009-08-13T16:16:00.000-07:002010-07-30T16:17:04.865-07:00Yuan Zhu joins the lab<a href="http://petrov.stanford.edu/people.html#yuan" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img alt="image" border="0" class="left" height="110" src="http://petrov.stanford.edu/images/Yuan.gif" width="120" /></a><strong class="style1"></strong><br />
<a href="http://petrov.stanford.edu/people.html#yuan">Yuan Zhu</a>, a second year graduate student from Genetics, is done with her rotations and has decided to join our lab. In her rotation project she studied evoltuion of prokaryotic genome size. It is not yet clear what she will focus on in her dissertation - she is broadly interested in the theoretical and experimental aspects of genome evolution, evolution of complex traits, and population genetics. She is hoping to combine experimental and theoretical/computation work in her thesis. We are all delighted with her choice!Petrov Labhttp://www.blogger.com/profile/17303400627666039056noreply@blogger.com0