Abstract
We are addressing three core questions in evolution:
How, and how frequently, do new genetic variants arise?
Why do some variants increase in frequency?
Why are some combinations of new variants incompatible?
These correspond to the fundamental evolutionary processes of mutation, selection and speciation, which we are studying using both bottom-up and top-down approaches. I will first demonstrate the power of second-generation sequencing, both in support of forward genetics (Schneeberger et al., Nat. Methods 2009), and in determining the rate and spectrum of spontaneous mutations (Ossowski et al., science 2010). Based on our experience with short-read sequencing (Ossowski et al., Genome Res. 2008), we have been advocating a 1001 genomes project for A. thaliana (http://1001genomes.org), and we have already sequenced 84 wild strains from this species. Interpretation of within-species polymorphism data is greatly facilitated by outgroup information from A. lyrata. Next, I will discuss a fitness trade-off we recently discovered. Allelic variants beneficial in one setting might be detrimental under different circumstances. plants vary greatly in their responses to pathogens, and this is thought to reflect fitness costs in the absence of pathogens or predators. We have found that allelic diversity at a single locus, ACCElErAtEd CEll dEAth 6 (ACd6) , underpins dramatic variation in both vegetative growth and resistance to microbial infection. ACd6 is also a causal factor for an autoimmune-like response that behaves as expected for dobzhansky-muller incompatibilities, which are often thought of underlying speciation events. together with other discoveries made by my group (bomblies et al., plos biol., 2007), this implicates the extreme allelic diversity of disease resistance genes (clark et al., science 2007), presumably due to pathogen pressures, as potential causes for the evolution of gene-flow barriers in plants.
