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How lineage selection and domestication in eudicot plants structures virulence and genomic variation in the fungus, Botrytis cinerea, and vice versa D. KLIEBENSTEIN (1) (1) University of California, Davis, U.S.A.
Host/pathogen interaction studies rely on the use of large effect models with pathogens that cause epidemic disease outbreaks. This has developed a model where interaction of proteins or metabolites from the host and pathogen trigger an “immune” response to create qualitative resistance. To test if this model applies to quantitative endemic pathogens, we study the molecular basis of host/pathogen interactions using the necrotrophic fungal pathogen Botrytis cinerea. Sequencing the genome of 96 diverse Botrytis cinerea isolates showed that high levels of genetic. Diversifying selection occurs at virulence loci such as toxin metabolite clusters and cell wall degrading genes and unknown loci that could be candidates for new virulence mechanisms. Extensive recombination in the genome shows that the species is not clonal and we can conduct GWA studies in the pathogen. Infecting all 96 isolates on Arabidopsis thaliana defense mutants with RNAseq showed that the pathogens genetic variation greatly alters the host’s transcriptional responses. The salicylate and jasmonate signaling pathways functioned as amplifiers of the response. Genome wide association mapping in the pathogen showed that there were no major effect loci in the pathogen and instead quantitative virulence on the pathogens side was as polygenic as quantitative resistance in the host. Genome wide association in Arabidopsis thaliana showed that resistance is highly polygenic and dependent on the genetics of the specific isolates. There was a slight but significant enrichment for R genes in this list, yet 95% of the causal genes were in other functional classes. We are currently infecting the entire collection of Botrytis on six other eudicot species to directly test how this plant/pathogen interaction has evolved. These results will be presented.
Abstract Number:
C6-2 Session Type:
Concurrent
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