Quantitative pathogenicity and host adaptation in a fungal plant pathogen revealed by whole-genome sequencing

Reda Amezrou (), Aurélie Ducasse, Jérôme Compain, Nicolas Lapalu, Anais Pitarch, Laetitia Dupont, Johann Confais, Henriette Goyeau, Gert H. J. Kema, Daniel Croll, Joëlle Amselem, Andrea Sanchez-Vallet and Thierry C. Marcel ()
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Reda Amezrou: Université Paris-Saclay, INRAE, UR BIOGER
Aurélie Ducasse: Université Paris-Saclay, INRAE, UR BIOGER
Jérôme Compain: Université Paris-Saclay, INRAE, UR URGI
Nicolas Lapalu: Université Paris-Saclay, INRAE, UR BIOGER
Anais Pitarch: Université Paris-Saclay, INRAE, UR BIOGER
Laetitia Dupont: Université Paris-Saclay, INRAE, UR BIOGER
Johann Confais: Université Paris-Saclay, INRAE, UR BIOGER
Henriette Goyeau: Université Paris-Saclay, INRAE, UR BIOGER
Gert H. J. Kema: Plant Research International B.V.
Daniel Croll: Department of Ecology and Evolution, Université de Neuchâtel
Joëlle Amselem: Université Paris-Saclay, INRAE, UR URGI
Andrea Sanchez-Vallet: CBGP, INIA, Campus de Montegancedo UPM, Pozuelo de Alarcón
Thierry C. Marcel: Université Paris-Saclay, INRAE, UR BIOGER

Nature Communications, 2024, vol. 15, issue 1, 1-14

Abstract: 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.

Date: 2024
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DOI: 10.1038/s41467-024-46191-1

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