Friday, May 19, 2017

On the non-random effects of random mutation

The idea that evolution produces (developmental) genetic architectures that make the effects of mutations biased towards particular phenotypes have come up a few times in recent discussions. Next week we will look a little closer at one of the models that have been used to explore the how and why of this problem.

10.00 in Darwin. Fika and entertainment provided.

 You can find the paper here

Epistasis and natural selection shape the mutational architecture of complex traits
Adam G Jones, Reinhard Burger & Stevan Arnold

The evolutionary trajectories of complex traits are constrained by levels of genetic variation as well as genetic correlations among traits. As the ultimate source of all genetic variation is mutation, the distribution of mutations entering populations profoundly affects standing variation and genetic correlations. Here we use an individual-based simulation model to investigate how natural selection and gene interactions (that is, epistasis) shape the evolution of mutational processes affecting complex traits. We find that the presence of epistasis allows natural selection to mould the distribution of mutations, such that mutational effects align with the selection surface. Consequently, novel mutations tend to be more compatible with the current forces of selection acting on the population. These results suggest that in many cases mutational effects should be seen as an outcome of natural selection rather than as an unbiased source of genetic variation that is independent of other evolutionary processes.

Thursday, May 11, 2017

Sex difference in lifespan and sexual conflict

For the next week's lab meeting, I would like to use this Drosophila paper as a case, to discuss  the evolution of sexual dimorphism in lifespan. 

Hope to hear your thoughts over fika!
Photo by Qinyang Li

Manipulation of feeding regime alters sexual dimorphism for lifespan and reduces sexual conflict in Drosophila melanogaster

 byElizabeth M. L. DuxburyWayne G. RostantTracey Chapman

Thursday, May 4, 2017

One gene to rule them all (in a phylogeny)?

To what extent can one gene (or a handful of them) affect a phylogeny? This paper suggest that even in very large data matrices the resolution of some branches can rely on tiny subsets of data. They show this to be the case in several contentious nodes of plant, animal and fungi data matrices and suggest a framework for quantifying the phylogenetic signal in such difficult cases. 

They also think that humans are more closely related to sponges than ctenophores, which is cool. 

Darwin, 9th of May, 10.00. Blueberry pie to compensate the phylogeny topic.

Contentious relationships in phylogenomic studies can be driven by a handful of genes

Phylogenomic studies have resolved countless branches of the tree of life, but remain strongly contradictory on certain, contentious relationships. Here, we use a maximum likelihood framework to quantify the distribution of phylogenetic signal among genes and sites for 17 contentious branches and 6 well-established control branches in plant, animal and fungal phylogenomic data matrices. We find that resolution in some of these 17 branches rests on a single gene or a few sites, and that removal of a single gene in concatenation analyses or a single site from every gene in coalescence-based analyses diminishes support and can alter the inferred topology. These results suggest that tiny subsets of very large data matrices drive the resolution of specific internodes, providing a dissection of the distribution of support and observed incongruence in phylogenomic analyses. We submit that quantifying the distribution of phylogenetic signal in phylogenomic data is essential for evaluating whether branches, especially contentious ones, are truly resolved. Finally, we offer one detailed example of such an evaluation for the controversy regarding the earliest-branching metazoan phylum, for which examination of the distributions of gene-wise and site-wise phylogenetic signal across eight data matrices consistently supports ctenophores as the sister group to all other metazoans.