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A gene-for-gene interaction involving a ‘late’ effector contributes to quantitative resistance to the stem canker disease in Brassica napus
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A gene-for-gene interaction involving a ‘late’ effector contributes to quantitative resistance to the stem canker disease in Brassica napus
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Journal Article
A gene-for-gene interaction involving a ‘late’ effector contributes to quantitative resistance to the stem canker disease in Brassica napus
2021
Overview
• 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.
Publisher
Wiley,Wiley Subscription Services, Inc,John Wiley and Sons Inc
Subject
