Abstracts (first author)
Using RAD-seq and candidate gene sequencing to explore patterns of heterozygosity at disease resistance genes across naturally inbred and outcrossed plant populations
Models of plant resistance (R) gene evolution suggest a significant role for balancing selection in maintaining high levels of genetic diversity. Selection can then act on this pool of resistance gene alleles to allow plant populations to recognise a diverse range of pathogen genotypes. However, the ecology and life history of a species can have strong effects on patterns of genetic diversity across the genome, which may counter the maintenance of genetic variation through selection. In particular, intraspecific variation in mating systems can produce naturally outcrossed and inbred populations, with reduced heterozygosity at neutral genetic loci in inbred populations. This reduction in heterozygosity is expected to occur throughout the genome, including at genes important for pathogen recognition and resistance, which may reduce the potential for rapid evolution of pathogen resistance in inbred populations.
The perennial plant, Arabidopsis lyrata, displays significant variation in mating system around the North American Great Lakes resulting in naturally outcrossed and inbred populations. Using Restriction Associated DNA (RAD) sequencing, we have genotyped 4 individuals from each of six inbreeding and six outcrossing populations of A. lyrata at ~ 30000 RAD loci. Using these sequence data, we can test for reduced heterozygosity across the genomes of individuals from inbred populations. We can also use these sequence data to estimate genetic diversity at or near candidate disease resistance genes (using comparisons to the well-annotated Arabidopsis thaliana genome). These analyses will be combined with sequence data produced via PCR amplification of particular resistance genes thought to be involved in the recognition of different pathogens of the Brassicaceae. Together these data should significantly improve our understanding of the genomic consequences of shifts in mating system and its potential effects on the evolution of disease resistance.