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Phytophthora blight, caused by the oomycete plant pathogen Phytophthora capsici, poses a significant risk to vegetable production globally. As P. capsici is readily dispersed in contaminated soil, water, and plant tissue, the recent increase in large-scale flooding events has resulted in a concomitant increase in Phytophthora blight incidence. We grow many of P. capsici‘s favorite hosts, e.g. pumpkins, eggplants, and string beans, here in New York, therefore, we have a keen interest in decoding P. capsici biology and improving disease management strategies. In collaboration with Chris Smart (Plant
Pathology and Plant-Microbe Biology Section) and Michael Mazourek (Plant Breeding and Genetics Section), we are taking a multi-faceted approach to achieve these goals.

Population genetic patterns of P. capsici are a complex function of reproductive mode (sexual or asexual), dispersal, host availability, and geography, among other variables. For example, lack of aerial dispersal results in significant genetic differentiation between closely spaced fields. To dissect how sexual and asexual reproduction influence an isolated P. capsici population, we analyzed pathogen samples collected from a controlled field population, located in Geneva, NY, over a 5-year time period. Founded by two known parents of opposite mating type, we traced changes in allele frequency and heterozygosity throughout the genome using single-nucleotide polymorphism (SNP) markers from 2009-13. Our recent manuscript provides insight into the role of sexual spore survival in delaying the onset of inbreeding, and details the influence of mating type on corresponding declines in heterozygosity. We continue to monitor allele frequency changes in the population.

We are also working at the interface of P. capsici-host interactions. Specifically, we are mapping quantitative trait loci (QTL) that confer partial tolerance to P. capsici in the squash species Cucurbita pepo. Complete resistance to the pathogen has not been identified in C. pepo, but variation for degree of susceptibility exists. We hypothesize that many QTL of small effect contribute to this variation. To detect these loci, we are using next-generation sequencing of pooled samples consisting of the extreme tolerant and susceptible tails of a very large F2 population.