Tag Archives: evolution

Genomic patterns of pleiotropy and the evolution of complexity (Wang et. al 2010)

ResearchBlogging.org

Posted by Victor Hanson-Smith, Conor O’Brien, and Bryn Gaertner.

One of the grand challenges of evo-devo is to understand how mutations of genetic sequences affect concomitant phenotypic traits.  Eighty-one years ago, Fisher (1930) proposed that every mutation may affect every trait, and the effect size of a gene on a trait is uniformly distributed: thus we should observe equal proportions of mutations causing large and small per-trait effects.  As a logical consequence of Fisher’s hypothesis, more complex organisms (that is, with more traits) should evolutionarily adapt to their environment at a slower rate than less complex organisms because the presence of more traits implies a higher density of gene-trait relationships and thus incurs a “cost of complexity” (Orr 2000).  However, it is widely accepted that organisms *do* evolve to be more complex, and populations of complex organisms successfully evolve towards fitness optima.  This implies the “cost of complexity” hypothesis is incorrect, or the cost is counteracted by some unknown force.

In contrast to a Fisherian view, contemporary evo-devo research widely accepts the general principle that genes interact in hierarchical modules to produce morphological and physiological traits.  A network-centric perspective of gene-trait interactions suggests that the effect of a particular mutation on downstream traits depends on the network location of the mutated gene: mutations in genes with high network centrality tend to be more pleiotropic because those genes affect many downstream traits, whereas mutations to peripheral genes are less pleiotropic.  However, the extent of modularity and pleiotropy across genomes is unknown.

A recently-published PNAS paper (Wang et al., 2010) repudiates the Fisher-Orr “cost of complexity” hypothesis and confirms contemporary intuition regarding genetic modularity using empirical data and an extension of an exiting model of adaptation.

Wang et al. analyzed genome-wide patterns of pleiotropy in three eukaryotes—yeast, mice, and nematodes—and observed significant modularity in the gene-trait relationship graph and generally low levels of pleiotropy for most genes.  This highly modular structure and generally low pleiotropy means that a mutation is more likely to be beneficial, as it is more likely to affect a small, related set of phenotypes in the same direction, as opposed to many phenotypes in random directions.

Moreover, the authors observed that pleiotropic mutations tend to have a larger per-gene effect than non-pleiotropic mutations.  By extending Orr’s “complexity cost” equation to allow for variable levels of pleiotropy, Wang et al. observed a small non-zero degree of pleiotropy actually increases—rather that impairs—the rate of adaptation. This is because the positive correlation between pleiotropy and effect size increases the probability of fixation and fitness gain in more complex organisms, i.e., those with greater complexity.  This result is important because it may explain the repeated evolution of complexity in many taxa.

Wang et al.’s analysis is based entirely on data mined from knock-out and RNAi experiments; their conclusions are consequently limited to the sequence space of null mutations that silence the function(s) of genes.  In contrast, a less-explored region of sequence space contains mutations that merely affect the relative activity of a gene’s protein product without entirely silencing the gene.  In non-null sequence space, the magnitude of a mutation’s effect is determined not only by the pleiotropy (a.k.a. the network centrality) of the mutated gene, but also the number of redundant pathways leading from that gene to a downstream phenotype.  It is widely accepted that pathway redundancy buffers traits from upstream changes in enzyme activity or dosage [see Kacser and Burns, “The Molecular Basis on Dominance”, Genetics 1981].  Whereas the effects of null mutations are strongly predicted by the extent of pleiotropy (as presently shown by Wang et al.), we hypothesize that the effect of a non-null mutation is largely predicted by the number of interaction pathways between the mutated gene and a downstream phenotype.  This counterhypothesis, however, has yet to be tested.

Read the paper by Wang et al., here:

Wang Z, Liao BY, & Zhang J (2010). Genomic patterns of pleiotropy and the evolution of complexity. Proceedings of the National Academy of Sciences of the United States of America, 107 (42), 18034-9 PMID: 20876104

Evolution 2010, day 4 roundup audiocast

Several authors from this blog are attending Evolution 2010. The conference is huge; with twelve concurrent sessions, it is impossible to see everything. In this audiocast, we discuss several noteworthy lectures from Day 4.

Download the audiocast here:

Evolution 2010, day 4 roundup audiocast (MP3, 22:17, 50.8 Mb)
The discussion panel includes: Victor Hanson-Smith, Paul Cziko, Julian Catchen, Conor O’Brien, Jeremy Yoder, Chris Smith, and Ingo Braasch.

Comments are welcome.

Evolution 2010, day 3 roundup audiocast

Several authors from this blog are attending Evolution 2010.  The conference is huge; with twelve concurrent sessions, it is impossible to see everything.  In this audiocast, we discuss several noteworthy lectures from Day 3.

Download the audiocast here:

Evolution 2010, day 3 roundup audiocast (MP3, 20:07, 49.1 Mb)

The discussion panel includes: Victor Hanson-Smith, Paul Cziko, Julian Catchen, Conor O’Brien, Jeremy Yoder, Chris Smith, and Ingo Braasch.

Comments are welcome.

Evolution 2010, day 2 roundup audiocast

Several authors from this blog are attending Evolution 2010.  The conference is huge; with twelve concurrent sessions, it is impossible to see everything.  In this audiocast, we discuss several noteworthy lectures from Day 2.

Download the audiocast here:

Evolution 2010, day 2 roundup audiocast (MP3, 20:07, 49.9 Mb)

The discussion panel includes: Victor Hanson-Smith, Paul Cziko, Julian Catchen, and Conor O’Brien.

Comments are welcome.

Evolution 2010, day 1 roundup audiocast

Several authors from this blog are attending Evolution 2010.  The conference is huge; with twelve concurrent sessions, it is impossible to see everything.  In this audiocast, we discuss several noteworthy lectures from Day 1.

Download the audiocast here:

Evolution 2010, day 1 roundup audiocast (MP3, 19:05, 45 Mb)

The discussion panel includes: Victor Hanson-Smith, Julian Catchen, Conor O’Brien, Bryn Gaertner, Chris Smith, and Jeremy Yoder.

Comments are welcome.

Mark Pagel at University of Oregon HBES conference

ResearchBlogging.org

Posted by Victor Hanson-Smith

Mark Pagel (MP) delivered a keynote lecture at the 22nd annual Human Behavior and Evolution Society conference, titled “The Rise of the Speaking Machine: Explorations in Language Evolution.”

MP has published several well-known papers on phylogenetic methods, speciation, and protein-protein networks, but his recent work investigates phylogeographic patterns of language expression [Pagel et al. 2007, Pagel 2008, Pagel et al. 2009].  This topic might seem eccentric for an EvoDevo blog, but I think the topic of language evolution is relevant to our interests for two reasons.  First, it reminds us that phylogenetic methods are useful for studying more than sequence data; rather, a phylogeny is useful for studying the evolution of any phenotype, including language.  Second, MP’s results strongly suggest that genetic evolution and linguistic evolution are governed by the same underlying patterns and processes; indeed, human language is simply a highly abstract phenotype.

MP’s hypothesis is that “language provides a digital regulatory mechanism for the newly emerged complex social phenotype of culuture.”  In other words, human language arose to regulate and vary our individual expression of the social phenotype, in a very similar way that the gene expression regulates the phenotype of cells.  If you missed MP’s lecture, you can absorb most of the content by reading the 2007 paper, 2008 paper, and 2009 paper.

Comments are welcome.

Pagel, M. (2009). Human language as a culturally transmitted replicator Nature Reviews Genetics DOI: 10.1038/nrg2560

EVO-WIBO 2010 highlights

Posted by Victor Hanson-Smith.

Several authors on this blog (including myself) just returned from Evo-Wibo 2010, a gathering of evolutionary biologists from the pacific northwest.  The talks were high-quality and covered a broad range of topics, from the macro (population and ecology interactions) to the micro (protein evolution).  I won’t summarize all twenty-seven talks, but allow me to highlight a few favorites:

Michael Doebli gave a talk titled “Complexity and Diversity,” which basically summarized his recent Science paper.  Michael’s main point is:

. . . if the ecological properties of an organism are determined by multiple traits with complex interactions, the conditions needed for frequency-dependent selection to generate diversity are relaxed to the point where they are easily satisfied in high-dimensional phenotype spaces.

Michael’s result is exciting because it sheds light on the origin of diversity.  Furthermore, the result seems obvious and leads me to wonder “why didn’t I think of that?”

Members of Bill Cresko’s lab (including Julian Catchen, Paul Hohenlohe, and Susan Bassham) gave a series of talks showcasing RAD tag sequencing [See here and here].  As a phylogeneticist, I am particularly interested in the potential to use RAD tags to identify sites that polymorphic within a population; these sites can be culled from phylogenetic analysis, thus removing a significant amount of “noise” when inferring inter-species phylogenies.

My final highlight is David Pollock‘s talk titled “Adaptation, Convergence, and Context-Dependent Evolution.”  David investigated why a very long phylogenetic branch leads to the snake clade.  One explanation is found in the large number of mitochondrial mutations allowing snakes to rapidly alter their metabolism in order to digest large meals.  I think David’s talk was interesting because it was the first (and only?) at this meeting to connect specific protein-level mutations to organism-level phenotypic changes.

Did you attend EVO-WIBO?  If so, I encourage your comments down below.  What presentations did you think were noteworthy?