A gene-for-gene interaction involving a 'late' effector contributes to quantitative resistance to the stem canker disease in Brassica napus.

Abstract

Summary The control of stem canker disease of Brassica napus (rapeseed), caused by the fungus Leptosphaeria maculans is based largely on plant genetic resistance: single‐gene specific resistance (Rlm genes) or quantitative, polygenic, adult‐stage resistance. Our working hypothesis was that quantitative resistance partly obeys the gene‐for‐gene model, with resistance genes ‘recognizing’ fungal effectors expressed during late systemic colonization.Five LmSTEE (stem‐expressed effector) genes were selected and placed under the control of the AvrLm4‐7 promoter, an effector gene highly expressed at the cotyledon stage of infection, for miniaturized cotyledon inoculation test screening of a gene pool of 204 rapeseed genotypes.We identified a rapeseed genotype, ‘Yudal’, expressing hypersensitive response to LmSTEE98. The LmSTEE98–RlmSTEE98 interaction was further validated by inactivation of the LmSTEE98 gene with a CRISPR‐Cas9 approach. Isolates with mutated versions of LmSTEE98 induced more severe stem symptoms than the wild‐type isolate in ‘Yudal’. This single‐gene resistance was mapped in a 0.6 cM interval of the ‘Darmor_bzh’ × ‘Yudal’ genetic map.One typical gene‐for‐gene interaction contributes partly to quantitative resistance when L. maculans colonizes the stems of rapeseed. With numerous other effectors specific to stem colonization, our study provides a new route for resistance gene discovery, elucidation of quantitative resistance mechanisms and selection for durable resistance.