RESUMO
KEY MESSAGE: A novel light intensity-dependent lesion mimic mutant with enhanced disease resistance was physiologically, biochemically, and genetically characterized, and the causative gene was fine mapped to a 1.28 Mbp interval containing 17 high-confidence genes. Lesion mimic mutants are ideal for studying disease resistance and programmed cell death photosynthesis in plants to improve crop yield. In this study, a novel light intensity-dependent lesion mimic mutant (MC21) was obtained from the wheat variety Chuannong16 (CN16) by ethyl methane sulfonate treatment. The mutant initially developed tiny lesion spots on the basal part of the leaves, which then gradually proceeded down to leaf sheaths, stems, shells, and awns at the flowering stage. The major agronomic traits were significantly altered in the mutant compared to that in the wild-type CN16. Furthermore, the mutant exhibited a lesion phenotype with degenerated chloroplast structure, decreased chlorophyll content, increased level of reactive oxygen species, and increased resistance to stripe rust and powdery mildew. Genetic analysis indicated that the lesion phenotype was controlled by a novel single semi-dominant nuclear gene. The target gene was mapped on chromosome arm 2AL located between Kompetitive Allele Specific PCR (KASP) markers, KASP-4211 and KASP-5353, and tentatively termed as lesion mimic 5 (Lm5). The fine mapping suggested that Lm5 was located in a 1.28 Mbp interval between markers KASP-5825 and KASP-9366; 17 high-confidence candidate genes were included in this genomic region. This study provides an important foundational step for further cloning of Lm5 using a map-based approach.