Assessing the impact of plant mating system and ploidy on adaptation to parasitism in changing environments

Host-pathogen interactions are dynamic systems that are influenced by factors that act on both interacting partners, either separately, or in response to one another. For example, changes in temperature or habitats can alter distributions of hosts and pathogens and thus bring new combinations of organisms into contact but can also change the virulence of pathogens or the responses of hosts. Many studies have focused on how direct interactions are altered by respective changes in immune recognition and pathogen avoidance systems but fewer have focused on how factors indirectly related to the interaction might affect the abilities of hosts and pathogens to coexist. A wide range of economically important plants vary in either mating system (inbreeding or outcrossing) or in ploidy level (many crops are polyploids, with more than two sets of chromosomes) from wild relatives but it has not been well studied how such changes affect pathogen response systems. Recent research on the genetic control of host-pathogen interactions in the economically important Brassicacaceae (which includes broccoli, rapeseed, and turnips) has tended to focus on the highly selfing model plant, Arabidopsis thaliana. While much has been learned from this, the lack of naturally occurring variation in genetic diversity, heterozygosity, mating system and ploidy level limits the potential to explore the effects of variation in host factors. A close relative, Arabidopsis lyrata, has sufficient variation across its range to investigate the effects of mating system and ploidy variation within a single species with a broad geographic distribution. We propose to investigate variation in response of A. lyrata to an important pathogen of both wild and cultivated Brassicaceae, oomycete pathogens in the genus Albugo, which cause a disease known as white blister rust. We propose to use a combination of laboratory and polytunnel field experiments to investigate how populations of A. lyrata sampled from different geographic regions and that differ in mating system or ploidy level vary in their responses to experimental infection with Albugo. We also plan to screen wild populations for natural variation in infection with Albugo and investigate the genetic basis for differences in responses using the latest in genomic sequencing technologies. We hope to establish whether: 1) resistance to these pathogens is reduced with inbreeding (which reduces genetic diversity and heterozgyosity within populations and could limit variation in pathogen response systems) or whether local adaptation to particular pathogens might instead make outcrossing less desirable (because recombining genomes from unrelated individuals could disrupt combinations of genes that allow effective pathogen response); 2) the duplication of pathogen response systems that would be expected to accompany whole genome duplication (polyploidy) confers an advantage (in terms of the diversity of pathogens that can be recognized or increased production of products necessary to combat pathogens), or whether the normal balance in pathogen response systems present in the diploid state might be disrupted by genome duplication; 3) whether the strength of host response systems vary along a latitudinal gradient (where temperature variation, length of growing season, rainfall and habitat types are likely to vary). A. lyrata tends to grow in low competition environments so we will also question whether exposure to pathogens hosted by other species, such as A. thaliana, might be involved in limiting their distributions and whether this varies in relation to prior exposure to the Albugo pathogen. Finally, we hope to uncover the genes responsible for regulating interactions between A. lyrata and Albugo and establish whether the same resistance mechanisms operate in host populations sampled from widely separated geographic regions and whether responses are similar to different strains of the pathogen.