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Protection of many crops is achieved through the use of genetic resistance.  Leptosphaeria maculans , the causal agent of blackleg disease of  Brassica napus , has emerged as a model for understanding gene‐for‐gene interactions that occur between plants and pathogens. Whilst many of the characterized avirulence effector genes interact with a single resistance gene in the host, the  AvrLm4‐7  avirulence gene is recognized by two resistance genes,  Rlm4  and  Rlm7 . Here, we report the “breakdown” of the  Rlm7  resistance gene in Australia, under two different field conditions. The first, and more typical, breakdown probably resulted from widescale use of  Rlm7 ‐containing cultivars whereby selection has led to an increase of individuals in the  L. maculans  population that have undergone repeat‐induced point (RIP) mutations at the  AvrLm4‐7  locus. This has rendered the  AvrLm4‐7  gene ineffective and therefore these isolates have become virulent towards both  Rlm4  and  Rlm7 . The second, more atypical, situation was the widescale use of  Rlm4  cultivars. Whilst a single‐nucleotide polymorphism is the more common mechanism of virulence towards  Rlm4 , in this field situation, RIP mutations have been selected leading to the breakdown of resistance for both  Rlm4  and  Rlm7 . This is an example of a resistance gene being rendered ineffective without having grown cultivars with the corresponding resistance gene due to the dual specificity of the avirulence gene. These findings highlight the value of pathogen surveillance in the context of expanded knowledge about potential complexities for Avr–R interactions for the deployment of appropriate resistance gene strategies.

molecular plant pathology

Independent breakdown events of the  Brassica napus Rlm7  resistance gene including via the off‐target impact of a dual‐specificity avirulence interaction