Fine mapping and phenotype assessment of the novel lesion mimic and early senescence lmes5 mutant in rice

Lesion mimic mutants spontaneously produce necrotic lesions similar to hypersensitive response in the absence of external stress. In this study, a novel lesion mimic and early senescence 5 (lmes5) mutant was identified after ethyl methanesulfonate mutagenesis. The mutant showed premature ageing at the mature stage, as well as the localized necrosis phenotype. Leaves of the lmes5 mutant showed decreased chlorophyll fluorescence, photosynthetic pigment contents, and net photosynthetic rate. In contrast, there was an increase in the number of dead cells, an accumulation of reactive oxygen species (hydrogen peroxide and hydroxyl radical), and decreased activities of superoxide dismutase and peroxidase. Consistent with these physiological changes, agronomic traits of the lmes5 mutant, such as plant height, percentage seed set, 1000-grain weight, and number of grains per panicle, were reduced. Consistent with the lesion mimic phenotype, there was an increase in expression of antioxidant reaction-related genes, and pathogenesis-related genes. Resistance to bacterial blight was enhanced and the spectrum of resistance to rice blast was broadened. In accordance with the phenotype of premature senescence, genes associated with chlorophyll synthesis and chloroplast development were inhibited, whereas genes associated with chlorophyll degradation were activated. Fine mapping revealed that the mutated gene was localized within a 116 kb interval on chromosome 4. At present, no lesion mimic genes have been reported in this region.

Automated summary

A novel lesion mimic mutant was identified in this study, which showed premature ageing and localized necrosis phenotype. The mutant had decreased photosynthetic function and agronomic traits, but enhanced resistance. Genes associated with antioxidant reaction, pathogenesis, and chlorophyll metabolism were found to be related to the mutant.