What are the conditions for multiple foci of adaptation?

Selection on standing variation, soft sweeps, parallel adaptation: these alternatives to the population genetics paradigm of the S-shaped selective sweep have in common the idea that the response of a species to a change in selection pressure may frequently involve multiple mutations, which may arise in multiple locales, and which may appear at different sites in the genome. Consequently, the footprint of selection in the genome is different to that expected under a single selective sweep and therefore likely to be missed by scans of the genome looking for selection.

Many examples of parallel adaptation have been put forward, for instance multiple drug resistance in the malaria parasite Plasmodium vivax. But how plausible is parallel adaptation as an evolutionary mechanism, and what are the conditions that make it likely? These questions were addressed by Graham Coop presenting joint work with his postdoc Peter Ralph in one of the stand-out talks of the SMBE conference in Lyon.

Their key finding is that the multifarious parameters that go into building a spatial model of adaptation (strength of selection, the mutation rate, population density, average dispersal distance of offspring) can be distilled down to a single key quantity: the characteristic length given by the equation

When the geographical extent of the species range exceeds this characteristic length, the conditions are right for parallel adaptation. Graham's talk made accessible the complex mathematics behind this result. He has kindly made the slides available (click here) and the paper is now available at the Genetics website (click here).

Visit to Kilifi

The final days in Paris were taken up by revisions to a paper submitted in April to PLoS Genetics. With luck the revisions will be accepted and that paper will be coming out soon. From Paris I flew to Mombasa, Kenya to begin a 3 week collaboration with Caroline Buckee at the KEMRI-Wellcome Trust research unit in Kilifi. Caroline, Pete Bull and others at Kilifi work on the evolution of var genes in Plasmodium falciparum, the most common and lethal agent of malaria. The var genes encode a family of proteins expressed by the pathogen on the membrane of infected red blood cells. Implicated in pathogenesis, these genes are highly diverse in order to evade the host immune system. The first step in piecing together their evolutionary history is to align the sequences - a task made difficult by the abundance of insertions and deletions. From there we hope to characterize the relative importance of gene duplication and homologous and non-homologous recombination in driving the evolution of these genes.