Whole-genome sequencing reveals diverse mechanisms underlying quantitative pathogenicity and host adaptation in a fungal plant pathogen
AMEZROU, R.; DUCASSE, A.; COMPAIN, J.; LAPALU, N.; PITARCH, A.; DUPONT, L.; CONFAIS, J.; GOYEAU, H.; KEMA, G. H.; CROLL, D.; AMSELEM, J.; SANCHEZ-VALLET, A.; MARCEL, T. C.
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Knowledge of genetic determinism and evolutionary dynamics mediating host-pathogen interactions is essential to manage fungal plant diseases. Studies on the genetic architecture of fungal pathogenicity often focus on large-effect effector genes triggering strong, qualitative resistance. It is not clear how this translates to predominately quantitative interactions. Here, we use the Zymoseptoria tritici-wheat model to elucidate the genetic architecture of quantitative pathogenicity and mechanisms mediating host adaptation. With a multi-host genome-wide association study, we identify 19 high-confidence candidate genes associated with quantitative pathogenicity. Analysis of genetic diversity reveals that sequence polymorphism is the main evolutionary process mediating differences in quantitative pathogenicity, a process that is likely facilitated by genetic recombination and transposable element dynamics. Finally, we use functional approaches to confirm the role of an effector-like gene and a methyltransferase in phenotypic variation. This study highlights the complex genetic architecture of quantitative pathogenicity, extensive diversifying selection and plausible mechanisms facilitating pathogen adaptation.
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