12 posts · 1,535 views
I am an evolutionary biologist, open access advocate, and professor at the University of California, Davis.
The Tree of Life
12 posts
Sort by Latest Post, Most Popular
View by Condensed, Full
- February 3, 2010
- 10:53 AM
- 123 views
Story behind the science: #PLoS Genetics "Evolutionary mirages" paper
by Jonathan Eisen in The Tree of Life
So there is this cool new paper out in PLoS Genetics: Evolutionary Mirages: Selection on Binding Site Composition Creates the Illusion of Conserved Grammars in Drosophila Enhancers. and I have wanted to write about it for a week or so. You see, the paper is about something I have been interested in for most of my career - how the particular processes by which mutations occur can sometimes be biased (i.e., some types of mutations are more common than others) and that these biases can create highly ordered patterns in genomes and in turn that observation of these ordered patters can sometimes be misinterpreted as being the result of adaptation. Mistaken claims of adaptation in genomics are a favorite topic of mine - and let me to create (with tongue in cheek) a new omics word - Adaptationomics.Anyway - so I really really like this paper. But there is a week bit of a problem in writing about it. You see, it is by my brother, Michael Eisen, a Prof. at UC Berkeley (and a student in his lab Richard Lusk). And, well, I don't want to say anything wrong or stupid about the paper since, well, my brother will be pissed off. And so I have not written about it yet. But then I realized the best way to write about this one is to simply ask my brother for the "Story behind the science" for the paper, as I have been doing for some other recent papers.If you want a summary of the paper, here it is in their own words:Authors summary: Because mutation is a random process, most biologists assume that apparently non-random features of genome sequences must be the result of natural selection acting to create and preserve them. Where this is true, genome sequences provide a powerful means to infer aspects of molecular, cellular, and organismal biology from the signatures of selection they have left behind. However, recent analyses have shown that many aspects of genome structure and organization that have traditionally been attributed to selection can often arise from random processes. Several groups—including ours—studying the sequences that specify when and where genes should be produced have identified common, seemingly conserved, architectural features, based on which we have proposed new models for the activity of the complex molecular machines that regulate gene expression. However, in the work described here we simulate the evolution of these regulatory sequences and show that many of the features that we and others have identified can arise as a byproduct of random mutational processes and selection for other properties. This calls into question many conclusions of comparative genome analysis, and more generally highlights what Michael Lynch has called the “frailty of adaptive hypotheses” for the origins of complex genomic structures.Conclusions: Lynch has eloquently argued that biologists are often too quick to assume that organismal and genomic complexity must arise from selection for complex structures and too slow to adopt non-adaptive hypotheses. Our results lend additional support to this view, and extend it to show that indirect and non-adaptive forces can not only produce structure, but also create an illusion that this structure is being conserved. We do not doubt that many aspects of transcriptional regulation constrain the location of transcription factor binding sites within enhancers. Indeed a large body of experimental evidence supports this notion, and we remain committed to identifying and characterizing these constraints. But if this process is to be fueled by comparative sequence analysis, as we believe it must be, it is essential that we give careful consideration to the neutral and indirect forces that we now know can produce evolutionary mirages of structure and function.I must say I love the title lead in "Evolutionary mirages" which is another but much better way of saying "Adaptationism is a bad thing". Anyway, before I get in any more trouble, here are some words about the paper from the Senior Author, Michael Eisen, my brother. Questions by me (I know, not very creative ones - but they will have to do):1. Why did you do this work?This paper started out as a control. My lab is interested in understanding how the enhancers that control gene expression work - focusing on those that control early development in Drosophila. In 2008, we published a paper showing that when we put enhancers from a distantly related family of flies into Drosophila melanogaster embryos, they drive patterns of expression that are identical to the endogenous D. melanogaster enhancers, even though they have almost no conservation of primary DNA sequence. But since they have the same function, they must have something in common - and so we compared the configurations of transcription factor binding sites in orthologous enhancers across different evolutionary timescales looking for something they shared.What we found is that binding sites in all of these enhancers occur in clusters. They are closer to each other than one would expect if they were scattered randomly in the ~1,000 bp of an enhancer. And, what's more, sites that were close to each other were far more likely to be conserved. Surely, we thought, this could be no accident. So we proposed that enhancers are organized into compact clusters of sites for one or more factors - and that these "mini modules" are the primary unit of enhancer function.But as we worked to extend these analyses to whole genomes, we sought a more rigorous, quantitative assessment, of just how improbably different levels of binding site clustering were. Like pretty much everyone in the field, we had used a null model in which binding sites were scattered randomly in an enhancer. But, I've been working with genomes long enough to know that nothing is ever truly random - and that all kinds of adaptive and non-adaptive processes create patterns in genome sequences that confound simple analyses. I wanted to come up with a null model for the distribution of sites within in an enhancer that was more realistic.To do this I turned to my graduate student Rich Lusk, a card-carrying population geneticist trained at the University of Chicago. Rich was proud of his status as one of the few members of the lab who didn't work on flies - but I convinced him to put aside the abstract models of binding site evolution in yeast and work on developing a real null model for our studies of enhancer evolution.The idea was to simulate enhancers evolving without any constraint on the organization of transcription factor binding sites they contain, and to see what happens. But this did not mean letting enhancers evolve neutrally - their extreme functional conservation demonstrates that they are under fairly strong constraint. Since it is pretty clear that these enhancers are responding to the same transcription factors in all of these species, Rich's simulations required that enhancers maintain their binding site composition - but placed no constraints on how the sites were organized relative to each other.And what we found was striking. Even with no explicit selection on binding site organization - these evolved enhancers had lots of structure! Binding sites were clustered together, and, the closer together sites were, the more conserved they were -- just like they were in real enhancers. In made us realize pretty quickly that the patterns we had latched onto - and which many other people were describing in different systems - might not be an evolutionary signature contraint on the organization of sites within in enhancers, but simply a byproduct of selection on binding site composition. If you want details, read the paper! But this has radically altered the way that we look at enhancer evolution.2. How did you come up with the title.Rich and I were writing the paper, and we had some really long, hideous, boring title. In writing the paper, the idea that things are not always what they appear to be was at the forefront of my mind. I was thinking about how desperate we and other people in the field were to figure out how enhancers work - it's a vexing problem that has defied decades of work - and how we all hoped that evolutionary analysis was going to rescue us - and how quickly and eagerly we latched on to the first signs of a signal - and how that was just like a mirage you see in the desert....3. Any interesting background? (see 1)4. When did the work start?About a year ago. We had been thinking about this for a while, but only when Rich focused on it did things get rolling.5. Why PLoS Genetics? Did PLoS Biology reject it?PLoS Genetics was our first choice. PG has become the premier journal for evolutionary genetics - it routinely publishes the most interesting and important work in the field, and everyone reads it. While every paper I've sent there has been heavily scrutinized, the editorial process has been fair (though sometimes agonizingly slow....), and each review has been thoughtful and many (including in this case) helped to vastly improve the paper.... Read more »
Lusk, R., & Eisen, M. (2010) Evolutionary Mirages: Selection on Binding Site Composition Creates the Illusion of Conserved Grammars in Drosophila Enhancers. PLoS Genetics, 6(1). DOI: 10.1371/journal.pgen.1000829
- January 26, 2010
- 06:29 PM
- 107 views
Wanted:Feedback on Importance of Finishing (Microbial) Genomes
by Jonathan Eisen in The Tree of Life
To allI am writing because I am working on a project to evaluate the importance of finishing microbial genomes. I know there has been lots of talk about this out there on the web and in papers, etc but I think a fresh discussion is useful. To get people up to speed below is a summary of the issue as I see it.Shotgun sequencing: Genome sequencing relies generally on the shotgun method at the beginning of a project where DNA fragments from an organism of interest are sequenced in a highly random manner.Assembly: After shotgun sequencing, the genome is assembled as best as possible into larger pieces (called contigs) and ordered sets of contigs (called scaffolds). All of this put together can be called an "assembly"Gaps: After the assembly phase, there are almost always gaps in the assembly. These generally come in two forms:sequencing gaps (where we know two contigs go together in some orientation but where we do not know the sequence of the DNA in between the contigs) physical gaps (where we have sets of scaffolds but do not know how the connect to each other). Quality: After the assembly phase, different components of the assembly can have different "qualities" where from example, some sections are somewhat ambiguous and others are highly reliableFinishing: Using any combination of laboratory, computational and other analyses one can both fill in gaps in the assembly and improve the quality of the assembly. This can generally be called "finishing"Quality of final product: Depending on the end quality of the assembly we could assign it to one of a few categories of "completeness" as outlined in a paper by Patrick Chain et al. In essence, you can consider the post to be a follow up to their paper and their work.We plan to try to measure what one gains by the finishing steps. We need to know this because we would like to make intelligent decisions about how to allocate resources. If one gains a lot from finishing then it would make sense to allocate significant resources to it. I note, I and some colleagues wrote a paper about this issue "The value of complete microbial genome sequencing (You get what you pay for)" that was published in 2002. This is without a doubt not the only discussion of the topic but I just wanted to point out I have been involved in this debate before. Despite that, I think we simply do not know right now what the benefits might be in the new sequencing landscape.------------------------------------------So the question I am asking here is:What do people think are the potential benefits that could come from finishing?------------------------------------------Here are some possible answers to get the discussion going:Gene discovery (e.g., there may be interesting/important genes in missing/low quality data)Esthetics of completeness (as in, it just feels better to have a finished genome)Improved analysis of genome organization (in particular from having contigs oriented correctly)Also - I note there has been some discussion of this for animals, plants etc (e.g., see recent paper by Eric Green and others on vertebrates) Many of the issues are similar but they are different enough that I think a microbe focused discussion is useful.Other links of interest:Discussion on Friendfeed to question from Michael BartonLANL finishing in the future meetingScivee talks from 2009 LANL meetingBlakesley, R., Hansen, N., Gupta, J., McDowell, J., Maskeri, B., Barnabas, B., Brooks, S., Coleman, H., Haghighi, P., Ho, S., Schandler, K., Stantripop, S., Vogt, J., Thomas, P., Comparative Sequencing Program, N., Bouffard, G., & Green, E. (2010). Effort required to finish shotgun-generated genome sequences differs significantly among vertebrates BMC Genomics, 11 (1) DOI: 10.1186/1471-2164-11-21Fraser, C., Eisen, J., Nelson, K., Paulsen, I., & Salzberg, S. (2002). The Value of Complete Microbial Genome Sequencing (You Get What You Pay For) Journal of Bacteriology, 184 (23), 6403-6405 DOI: 10.1128/JB.184.23.6403-6405.2002Chain, P., & et al. (2009). Genome Project Standards in a New Era of Sequencing Science, 326 (5950), 236-237 DOI: 10.1126/science.1180614Friendfeed discussion of this post:
--------
This is from the "Tree of Life Blog"
of Jonathan Eisen, an evolutionary biologist and Open Access advocate
at the University of California, Davis. For short updates, follow me on Twitter.
--------
... Read more »
Blakesley, R., Hansen, N., Gupta, J., McDowell, J., Maskeri, B., Barnabas, B., Brooks, S., Coleman, H., Haghighi, P., Ho, S.... (2010) Effort required to finish shotgun-generated genome sequences differs significantly among vertebrates. BMC Genomics, 11(1), 21. DOI: 10.1186/1471-2164-11-21
Fraser, C., Eisen, J., Nelson, K., Paulsen, I., & Salzberg, S. (2002) The Value of Complete Microbial Genome Sequencing (You Get What You Pay For). Journal of Bacteriology, 184(23), 6403-6405. DOI: 10.1128/JB.184.23.6403-6405.2002
Chain, P., & et al. (2009) Genome Project Standards in a New Era of Sequencing. Science, 326(5950), 236-237. DOI: 10.1126/science.1180614
- January 26, 2010
- 12:32 PM
- 137 views
Cool paper, & winner of "worst new omics word award": Predatosome
by Jonathan Eisen in The Tree of Life
And the bad new omics words keep streaming in. Today's winner of the "Worst New Omics Word Award" is going to Carey Lambert, Chien-Yi Chang, Michael J. Capeness and R. Elizabeth Sockett from Nottingham for their use/ invention of "Predatosome". They use this term in the title of their new PLoS One paper: The First Bite— Profiling the Predatosome in the Bacterial Pathogen Bdellovibrio. Here is the very long sentence where the define it:The gene products required for the initial invasive predatory processes have not been extensively studied but the genome sequencing of B. bacteriovorus HD100 [1] revealed a genome of 3.85Mb, including a core genome similar to that of non-predatory bacteria and some 40% of the genome comprising a potential predicted “predatosome” of genes, encoding both hydrolytic products that may be employed in prey degradation, and genes that may be required specifically for host predation and thus are not conserved across the Proteobacteria.The paper is actually quite interesting. They use genomic approaches to characterize a fascinating organism - the bacterial species Bdellovibrio bacteriovorus. This bug is a predatory organism - eating other bacteria. Since it eats them from the inside out, some, including these authors, refer to this organism as a pathogen of other bacteria and their is some discussion here and elsewhere for its potential to serve as a "living antibiotic" in much the same way people are trying to use bacterial viruses (a.k.a. phage).The paper overall is quite nice on first read. They used microarray studies to characterize gene expression patterns in different phases of the life cycle (see Figure above for the life cycle outline). They backed up this work by quantitative PCR studies and regular RT PCR. And based upon their analysis they found some genes that are "Up-Regulated in Predatory, but Not HI" phase (HI stands for host-independent). And here is where they really tell us what they mean by predatosome:This category of 240 genes are very interesting as they potentially exclude those genes simply involved with release from attack-phase into growth, namely they should be part of the “predatosome” of predatorily specific genes.It seems to me this terminology is completely unnecessary. All they need to do is say they are studying the genes related to the predatory phase. To assign these genes to the "predatosome" is a bit much. They continue in the paper to report some really interesting stuff. For example, they also examine another predatory bacterial species, and look at whether there are genes conserved in the process between species. They made some really nice figures by the way about the different phases of hte life cycle in this organism and which genes are expressed:Anyway - the science in the paper is nice. However, the invention of yet another omics word is a bit much. And thus Lambert et al. are winners of the highly coveted "Worst New Omics Word Award" for their invention of "predatosome". Details on the paper are below - and that is where the figures come from too. (Hat tip to Bora for letting me know about the paper, and the word).Lambert, C., Chang, C., Capeness, M., & Sockett, R. (2010). The First Bite— Profiling the Predatosome in the Bacterial Pathogen Bdellovibrio PLoS ONE, 5 (1) DOI: 10.1371/journal.pone.0008599Friendfeed comments below:
--------
This is from the "Tree of Life Blog"
of Jonathan Eisen, an evolutionary biologist and Open Access advocate
at the University of California, Davis. For short updates, follow me on Twitter.
--------
... Read more »
Lambert, C., Chang, C., Capeness, M., & Sockett, R. (2010) The First Bite— Profiling the Predatosome in the Bacterial Pathogen Bdellovibrio. PLoS ONE, 5(1). DOI: 10.1371/journal.pone.0008599
- January 20, 2010
- 06:57 AM
- 119 views
Confronting Intelligent Design arguments directly in the scientific literature
by Jonathan Eisen in The Tree of Life
... Read more »
FARMER, M., & HABURA, A. (2010) Using Protistan Examples to Dispel the Myths of Intelligent Design. Journal of Eukaryotic Microbiology, 57(1), 3-10. DOI: 10.1111/j.1550-7408.2009.00460.x
- January 6, 2010
- 12:32 PM
- 124 views
#PLoSOne paper keywords revealing: (#Penis #Microbiome #Circumcision #HIV); press release misleading
by Jonathan Eisen in The Tree of Life
UPDATE - READ COMMENTS - LEAD AUTHOR HAS GOTTEN PRESS RELEASE CHANGED
A new paper just showed up on PLoS One and it has some serious potential to be important The paper (PLoS ONE: The Effects of Circumcision on the Penis Microbiome) reports on analyses that show differences in the microbiota (which they call the microbiome - basically what bacterial species were present) in men before and after circumcision. And they found some significant differences. It is a nice study of a relatively poorly examined subject - the bacteria found on the penis w/ and w/o circumcision. This is a particularly important topic in light of other studies that have shown that circumcision may provide some protection against HIV infection.
In summary here is what they did - take samples from men before and after circumcision. Isolate DNA. Run PCR amplification reactions to amplify variable regions of rRNA genes from these samples. Then conduct 454 sequencing of these amplified products. And then analyze the sequences to look at the types and #s of different kinds of bacteria.
What they found is basically summarized in their last paragraph
"This study is the first molecular assessment of the bacterial diversity in the male genital mucosa. The observed decrease in anaerobic bacteria after circumcision may be related to the elimination of anoxic microenvironments under the foreskin. Detection of these anaerobic genera in other human infectious and inflammatory pathologies suggests that they may mediate genital mucosal inflammation or co-infections in the uncircumcised state. Hence, the decrease in these anaerobic bacteria after circumcision may complement the loss of the foreskin inner mucosa to reduce the number of activated Langerhans cells near the genital mucosal surface and possibly the risk of HIV acquisition in circumcised men."
And this all sounds interesting and the work seems solid. I note that some friends / colleagues of mine were involved in this including Jacques Ravel who used to be at TIGR and now is at U MD and Paul Kiem who is associated with TGen in Arizona. For anyone interested in HIV, the human microbiome, circumcision, etc, it is probably worth looking at.
However, the press release I just saw from TGen really ticked me off. The title alone did me in "Study suggests why circumcised men are less likely to become infected with HIV". Sure the study did suggest a possible explanation for why circumcised men are less likely to get HIV infections - the paper was justifiably VERY cautious about this inference. They basically state that there are some correlations worth following up.
The press release goes on to say "The study ... could lead to new non-surgical HIV preventative strategies for the estimated 70 percent of men worldwide (more than 2 billion) who, because of religious or cultural beliefs, or logistic or financial barriers, are not likely to become circumcised." Well sure, I guess you could say that. I think they are iplying you could change the microbiome somehow and therefore protect from HIV but that implies (1) that there really is a causal relationship between the microbial differences in HIV protection and (2) that one could change the microbiome easily, which is a big big stretch given how little we know right now.
Anyway - the science seems fine and not over-reaching. But the press release is annoying and misleading. Shocking I know. But this one got to me.
UPDATE - SEE COMMENTS HERE AND IN FRIENDFEED. LEAD AUTHOR GOT PRESS RELEASE CHANGED.
Price, L., Liu, C., Johnson, K., Aziz, M., Lau, M., Bowers, J., Ravel, J., Keim, P., Serwadda, D., Wawer, M., & Gray, R. (2010). The Effects of Circumcision on the Penis Microbiome PLoS ONE, 5 (1) DOI: 10.1371/journal.pone.0008422
--------
This is from the "Tree of Life Blog"
of Jonathan Eisen, an evolutionary biologist and Open Access advocate
at the University of California, Davis. For short updates, follow me on Twitter.
--------... Read more »
Price, L., Liu, C., Johnson, K., Aziz, M., Lau, M., Bowers, J., Ravel, J., Keim, P., Serwadda, D., Wawer, M.... (2010) The Effects of Circumcision on the Penis Microbiome. PLoS ONE, 5(1). DOI: 10.1371/journal.pone.0008422
- December 29, 2009
- 02:03 PM
- 160 views
Story Behind the Nature Paper on 'A phylogeny driven genomic encyclopedia of bacteria & archaea' #genomics #evolution
by Jonathan Eisen in The Tree of Life
Today is a fun day for me. A paper on which I am the senior author is being published in Nature (yes, the Academic Editor in Chief of PLoS Biology is publishing a paper in Nature, more on that below ..). This paper, entitled, "A phylogeny driven genomic encyclopedia of bacteria and archaea" represents a culmination of years of work by many people from multiple institutions. Today in this blog I am going to do my best to tell the story behind the paper - about the people and the process and a little bit about the science.
First, a brief bit about the science in the paper. In this paper, we (mostly people at the Joint Genome Institute, where I have an Adjunct Appointment -- but also people in my lab at UC Davis and at the DSMZ culture collection) did a relatively simple thing - we started with the rRNA tree of life as a guide. Then we identified branches in the bacterial and archaeal portions of this tree where there were no genome sequences available (or in progress) (this was done mostly by Phil Hugenholtz, Dongying Wu and Nikos Kyrpides) Next we searched for representatives of these "unsequenced" branches in the DSMZ culture collection (a collection of bacteria and archaea that can be grown in the lab). And we identified in total some 200 of these. And then the DSMZ (under the direction of Hans-Peter Klenk) grew these organisms and sent the DNA to the Joint Genome Institute. And then JGI turned on their genome sequencing muscle and sequenced the genomes of the organisms in the DNA samples. And finally, we spent a good deal of time then analyzing the data asking a pretty simple question - are there any general benefits that come from this "phylogeny driven" approach to sequencing genomes compared to what one might find with sequencing just any random genome (after all, any genome sequence could have some value)? The paper, describes what we found, which is that there are in fact many benefits that come from sequencing genomes from branches in the tree for which genomes are not available.
More on the details of the science below. But first, I want to note that this paper was truly an amazing team effort, with all sorts of people from the JGI in particular, going above and beyond the call of duty to make sure it happened and worked well. And the Department of Energy has been truly phenomenal in my opinion in supporting this project which in the end is not explicitly about "energy" per se but is really about providing a reference set of genomes that should improve the value of all microbial genome data.
Anyway, now for the story behind the story. And be prepared, because this is a bit long. But I think it is important to place this work in a bigger context both in terms of my background as well as some of the background of other people in the project. If you can't wait for more on the GEBA project then perhaps you should go to some of these links:
Videos of talks I have given on the project:
"Genomic Encyclopedia of Bacteria and Archaea (GEBA)"- Jonathan ...
Recent talk I gave at the Sackler NAS "Microbes and Health" meeting
Podcast of interview of me for ASM's Meet the scientist
Stories about GEBA
Nature News from 11.17.2009
Stories about our paper
Nature News
GenomeWeb "GEBA Researchers Publish Results from Dozens of Bacterial, Archaeal Genomes"
Ars Technica article "Presenting a genomic encyclopedia of bacteria (and archaea" by John Timmer
Iddo Friedberg blogged about it
The OpenHelix Blog on it
Leonardo Martins blogs about it here and helps translate a Spanish story about the project
R&D magazine has a post based on the press releases here
NY Times story by Carl Zimmer here.
FriendFeed Discussions here (includes a thread about Nature using a Creative Commons license)
And I will post more links as they come up. Below what I try to provide is some of the story behind the story:
My personal interest in applied uses of phylogenetics stage 1: undergraduate preparation at Harvard
As this paper is primarily about an applied use of phylogenetics (in selecting genomes for sequencing), I thought it would be worth going into some of how I personally became a bit obsessed with applied uses of phylogenetics. For me, my obsession began as an undergraduate at Harvard where I got exposed to the value of phylogeny as a tool from many many angles including but not limited to:
Freshman year taking a course taught by Stephen Jay Gould where Wayne and David Maddison were Teaching Assistant's and where they were demoing their new phylogenetics software called MacClade
Sophomore year taking a conservation biology class with Eric Fajer and Scott Melvin where I was exposed to the concept of "phylogenetic diversty" as a tool in assessing conservation plans
Junior year working in the lab of Fakhri Bazzaz with people like David Ackerly and Peter Wayne who made use of phylogeny as a key tool in their research projects
Senior year and the year after graduating where I worked in the lab of Colleen Cavanaugh using rRNA based phylogenetic analysis to characterize uncultured chemosynthetic symbionts. I note it was in Colleen's lab that I also became obsessed you could say with microbes and why they rock.
My personal interest in applied uses of phylogenetics stage 2: graduate school at Stanford
All of this and more gave me a strong passion for phylogeny as a tool. And so when I went to graduate school at Stanford (originally to work with Ward Watt on butterflies, but then I switched to working in Phil Hanawalt's lab on the "Evolution of DNA repair genes, proteins and processes"). And while in that lab I become pretty much obsessed with three things, all related to phylogeny.
First, I was interested in whether the rRNA tree of life, which I had used in my studies in Colleen Cavanaugh's lab (and in my first paper in J. Bacteriology, which, thanks to ASM, is now in Pubmed Central and free at ASM's site too), was robust or, as some critics argued, was not that useful. This was a critical question since the best way to study the phylogeny of microbes at the time, and also the best way to study uncultured microbes, was to leverage the ability to clone rRNA genes by PCR and then to build evolutionary trees of those rRNA genes. As part of my graduate work, I did a study where I compared the phylogenetic trees of rRNA to trees of another gene from the same speci... Read more »
Wu, D., Hugenholtz, P., Mavromatis, K., Pukall, R., Dalin, E., Ivanova, N., Kunin, V., Goodwin, L., Wu, M., Tindall, B.... (2009) A phylogeny-driven genomic encyclopaedia of Bacteria and Archaea. Nature, 462(7276), 1056-1060. DOI: 10.1038/nature08656
- December 29, 2009
- 01:43 AM
- 164 views
More coverage of the GEBA "Phylogeny Driven Genomic Encyclopedia"
by Jonathan Eisen in The Tree of Life
Additional discussion of recent paper... Read more »
Wu, D., Hugenholtz, P., Mavromatis, K., Pukall, R., Dalin, E., Ivanova, N., Kunin, V., Goodwin, L., Wu, M., Tindall, B.... (2009) A phylogeny-driven genomic encyclopaedia of Bacteria and Archaea. Nature, 462(7276), 1056-1060. DOI: 10.1038/nature08656
- December 24, 2009
- 08:04 AM
- 135 views
Story Behind the Nature Paper on 'A phylogeny driven genomic encyclopedia of bacteria & archaea' #genomics #evolution
by Jonathan Eisen in The Tree of Life
Discussion of the background to a recent Nature paper ... Read more »
Wu, D., Hugenholtz, P., Mavromatis, K., Pukall, R., Dalin, E., Ivanova, N., Kunin, V., Goodwin, L., Wu, M., Tindall, B.... (2009) A phylogeny-driven genomic encyclopaedia of Bacteria and Archaea. Nature, 462(7276), 1056-1060. DOI: 10.1038/nature08656
- December 22, 2009
- 12:00 AM
- 137 views
Story behind the story for new #PLoSOne paper on Bayesian phylogenetics
by Jonathan Eisen in The Tree of Life
There is an interesting new paper in PLoS One" Long-Branch Attraction Bias and Inconsistency in Bayesian Phylogenetics" by Brian Kolaczkowski and Joseph Thornton. The work focuses on methods for inferring phylogenetic history and in particular two types of statistical approaches: Likelihood and Bayesian. These methods are related to each other in that both attempt to use statistical models of evolution and then test different possible phylogenetic trees related taxa by how well certain data sets about those taxa map into the different possible trees. What they did in this new paper was test, with some simulations, and with some mathematical analyses. And somewhat surprisingly, they find that Bayesian methods, which have become more popular recently, appear to be more prone to errors than likelihood methods, when the data sets have multiple not closely related taxa with long branches. (Note if you want to learn more about phylogenetic methods, you can look at the online chapter (html format or PDF) from my Evolution Textbook, though I confess this needs a bit of revision, which I am working on now).... Read more »
Kolaczkowski, B., & Thornton, J. (2009) Long-Branch Attraction Bias and Inconsistency in Bayesian Phylogenetics. PLoS ONE, 4(12). DOI: 10.1371/journal.pone.0007891
- October 29, 2009
- 01:24 PM
- 126 views
More on the PLoS Special Collection on the Genomic of Emerging Infectious Diseases
by Jonathan Eisen in The Tree of Life
Discussion of new PLoS Series on Genomics of Emerging Infectious Diseases... Read more »
Eisen, J., & MacCallum, C. (2009) Genomics of Emerging Infectious Disease: A PLoS Collection. PLoS Biology, 7(10). DOI: 10.1371/journal.pbio.1000224
- November 24, 2008
- 12:00 AM
- 104 views
Open Microbial Diversity: PLoS papers on using 454-Roche pyrosequencing for rRNA studies
by Jonathan Eisen in The Tree of Life
Discussion of two new papers on 454 sequencing and microbial diversity... Read more »
Huse, S., Dethlefsen, L., Huber, J., Welch, D., Relman, D., & Sogin, M. (2008) Exploring Microbial Diversity and Taxonomy Using SSU rRNA Hypervariable Tag Sequencing. PLoS Genetics, 4(11). DOI: 10.1371/journal.pgen.1000255
Dethlefsen, L., Huse, S., Sogin, M., & Relman, D. (2008) The Pervasive Effects of an Antibiotic on the Human Gut Microbiota, as Revealed by Deep 16S rRNA Sequencing. PLoS Biology, 6(11). DOI: 10.1371/journal.pbio.0060280
- October 13, 2006
- 12:00 AM
- 99 views
World's Smallest Genome of a Cellular Organism?
by Jonathan Eisen in The Tree of Life
Discussion of Science paper on a very small genome... Read more »
Nakabachi, A., Yamashita, A., Toh, H., Ishikawa, H., Dunbar, H., Moran, N., & Hattori, M. (2006) The 160-Kilobase Genome of the Bacterial Endosymbiont Carsonella. Science, 314(5797), 267-267. DOI: 10.1126/science.1134196
topics
join us!
Do you write about peer-reviewed research in your blog? Use ResearchBlogging.org to make it easy for your readers — and others from around the world — to find your serious posts about academic research.
If you don't have a blog, you can still use our site to learn about fascinating developments in cutting-edge research from around the world.
News
Editor's selections: corporate water abuse, vanishing audiophiles, artificial coffee smelling and 60k-year-old canteens
Editor's Selections: An asteroid killed the dinosaurs, innate immunity and obesity, and vaccinia virus in Brazil
Exploitation Nation: Cheating Microbes, Parasites, and Your Colon
