Abstract

AbstractSenescence in plants is a complex and highly regulated process. However, the early senescence of leaf directly affects crop yield and quality. Identifying early senescence mutants and understanding its mechanism are critical to crop genetic improvement. In this study, we isolated an early senescence mutant esl13 (early senescence leaf 13) by ethyl methane sulfonate mutagenesis of Xinong 1B. Under paddy field conditions, the leaves of esl13 are normal green at the tillering stage, yellow at the booting stage, and gradually extended to the base of the leaves, and the senescence was most severe at the mature stage. At the booting stage, the leaves of mutant showed significantly lower photosynthetic pigment content, weaker chloroplast autofluorescence, and a highly significant reduction in net photosynthetic rate, resulting in shorter plants heights, shorter spike length, and lower seed yield at the mature stage. Similarly, the activity of antioxidant enzymes catalase, superoxide dismutase, and peroxidase decreased continuously, and malondialdehyde and superoxide anion (O2−) accumulated in the mutant esl13. Genetic analysis showed that the leaf senescence phenotype of esl13 is controlled by a single recessive nuclear gene, which was fine mapped between two molecular markers insertion‐deletion 4‐4 and SNP220 on chromosome 4. Gene sequencing showed that the 1230th base starting from ATG of the candidate gene LOC_Os04g48530 changed from T to A, causing the encoded amino acid change. Genetic complementation experiments confirmed the gene LOC_Os04g48530 controlled the mutant phe notype. This research provides new clues for further elucidating the regulation mechanism of rice senescence.

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