生物
遗传建筑学
遗传学
适应(眼睛)
效应器
进化动力学
基因组
致病性
数量性状位点
遗传变异
寄主(生物学)
基因
转座因子
计算生物学
人口
微生物学
神经科学
人口学
社会学
细胞生物学
作者
Reda Amezrou,Aurélie Ducasse,Jérôme Compain,Nicolas Lapalu,Anaïs Pitarch,Laëtitia Dupont,Johann Confais,Henriette Goyeau,G.H.J. Kema,Daniel Croll,Joëlle Amselem,Andrea Sánchez‐Vallet,Thierry C. Marcel
标识
DOI:10.1038/s41467-024-46191-1
摘要
Abstract 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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