Saturday, October 16, 2010

Selection in fruitflies - what kind of genomic signatures does it leave?

We are pretty confident that we know what signatures of selection look like for some loci in humans (skin color, lactase etc...) but how about less clear-cut/subtle cases which may represent the majority of cases? This experiment gives us some much needed insight into what signatures of selection we might expect for most instances of natural selection.

Genome-wide analysis of a long-term evolution experiment with Drosophila

Molly K. Burke, Joseph P. Dunham, Parvin Shahrestani, Kevin R. Thornton, Michael R. Rose & Anthony D. Long
Nature 2010
Abstract: Experimental evolution systems allow the genomic study of adaptation, and so far this has been done primarily in asexual systems with small genomes, such as bacteria and yeast. Here we present whole-genome resequencing data from Drosophila melanogaster populations that have experienced over 600 generations of laboratory selection for accelerated development. Flies in these selected populations develop from egg to adult ~20% faster than flies of ancestral control populations, and have evolved a number of other correlated phenotypes. On the basis of 688,520 intermediate-frequency, high-quality single nucleotide polymorphisms, we identify several dozen genomic regions that show strong allele frequency differentiation between a pooled sample of five replicate populations selected for accelerated development and pooled controls. On the basis of resequencing data from a single replicate population with accelerated development, as well as single nucleotide polymorphism data from individual flies from each replicate population, we infer little allele frequency differentiation between replicate populations within a selection treatment. Signatures of selection are qualitatively different than what has been observed in asexual species; in our sexual populations, adaptation is not associated with ‘classic’ sweeps whereby newly arising, unconditionally advantageous mutations become fixed. More parsimonious explanations include ‘incomplete’ sweep models, in which mutations have not had enough time to fix, and ‘soft’ sweep models, in which selection acts on pre-existing, common genetic variants. We conclude that, at least for life history characters such as development time, unconditionally advantageous alleles rarely arise, are associated with small net fitness gains or cannot fix because selection coefficients change over time.
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