The wheat lesion mimic 34 mutant shows lesion mimicry and enhanced reactive oxygen species-mediated immunity to powdery mildew

Abstract Lesion mimicry typically manifests as leaf disease-like symptoms in the absence of pathogen infection, characterized by a hypersensitive response (HR), which is intricately linked to plant disease resistance. In this study, the wheat (Triticum aestivum L) mutant lesion mimic 34 (lm34), harboring a recessive mutation in the Zhongyou 206 (ZY206) background, was comprehensively investigated. The lm34 mutation was mapped to a 140-kb region on chromosome 4AL through bulked segregant exome capture sequencing (BSE-Seq) and fine-mapping. Sequence comparison and phenotypic analysis of the lm34Jing mutant revealed that TraesCS4A03G1225400, encoding a typical CC-NB-LRR protein, is the causal gene in lm34. Transient expression assays in Nicotiana benthamiana leaves indicated that the TaLM34 extended coiled coil (eCC) domain can induce cell death. Furthermore, lm34 mutants display elevated reactive oxygen species (ROS) levels and significantly increased expression of pathogenesis-related (PR) genes (PR2 and PR10), leading to enhanced powdery mildew resistance. Our findings suggest that TaLM34 can serve as a potential target for the development of wheat cultivars with improved disease resistance. Overall, our study sheds light on the molecular mechanisms underlying wheat disease resistance and cell death.