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A fungal avirulence factor encoded in a highly plastic genomic region triggers partial resistance to septoria tritici blotch
Author(s) -
Meile Lukas,
Croll Daniel,
Brunner Patrick C.,
Plissonneau Clémence,
Hartmann Fanny E.,
McDonald Bruce A.,
SánchezVallet Andrea
Publication year - 2018
Publication title -
new phytologist
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.742
H-Index - 244
eISSN - 1469-8137
pISSN - 0028-646X
DOI - 10.1111/nph.15180
Subject(s) - pathosystem , biology , genetics , gene , mycosphaerella graminicola , genome , plant disease resistance , effector , population , septoria , allele , comparative genomics , transposable element , genomics , botany , demography , sociology , microbiology and biotechnology
Summary Cultivar‐strain specificity in the wheat– Zymoseptoria tritici pathosystem determines the infection outcome and is controlled by resistance genes on the host side, many of which have been identified. On the pathogen side, however, the molecular determinants of specificity remain largely unknown. We used genetic mapping, targeted gene disruption and allele swapping to characterise the recognition of the new avirulence factor Avr3D1. We then combined population genetic and comparative genomic analyses to characterise the evolutionary trajectory of Avr3D1 . Avr3D1 is specifically recognised by wheat cultivars harbouring the Stb7 resistance gene, triggering a strong defence response without preventing pathogen infection and reproduction. Avr3D1 resides in a cluster of putative effector genes located in a genome region populated by independent transposable element insertions. The gene was present in all 132 investigated strains and is highly polymorphic, with 30 different protein variants identified. We demonstrated that specific amino acid substitutions in Avr3D1 led to evasion of recognition. These results demonstrate that quantitative resistance and gene‐for‐gene interactions are not mutually exclusive. Localising avirulence genes in highly plastic genomic regions probably facilitates accelerated evolution that enables escape from recognition by resistance proteins.