SPL50 Regulates Cell Death and Resistance to Magnaporthe Oryzae in Rice

Background The identification of spotted leaf 50 ( spl50 ), a novel lesion mimic mutant (LMM) in rice, provides critical insights into the mechanisms underlying programmed cell death (PCD) and innate immunity in plants. Results Based on ethyl methane sulfonate (EMS)-induced mutagenesis, the spl50 mu...

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Published inRice (New York, N.Y.) Vol. 17; no. 1; pp. 51 - 14
Main Authors Ruan, Banpu, Wu, Hui, Jiang, Yaohuang, Qiu, Jiehua, Chen, Fei, Zhang, Yanli, Qiao, Yu, Tang, Mingyue, Ma, Yingying, Qian, Qian, Wu, Limin, Yu, Yanchun
Format Journal Article
LanguageEnglish
Published New York Springer US 13.08.2024
Springer Nature B.V
SpringerOpen
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Summary:Background The identification of spotted leaf 50 ( spl50 ), a novel lesion mimic mutant (LMM) in rice, provides critical insights into the mechanisms underlying programmed cell death (PCD) and innate immunity in plants. Results Based on ethyl methane sulfonate (EMS)-induced mutagenesis, the spl50 mutant mimics hypersensitive responses in the absence of pathogen by displaying spontaneous necrotic lesions after the tillering phase. SPL50, an ARM repeat protein essential for controlling reactive oxygen species (ROS) metabolism and boosting resistance to blast disease, was identified by map-based cloning techniques. This work also demonstrates the detrimental effects of spl50 on photosynthetic efficiency and chloroplast development. The crucial significance of SPL50 in cellular signaling and stress response is shown by its localization to the cytoplasm and constitutive expression in various plant tissues. In light of growing concerns regarding global food security, this study highlights the pivotal role of SPL50 in regulating programmed cell death (PCD) and enhancing the immune response in plants, contributing to strategies for improving crop disease resistance. Conclusions The novel identification of the SPL50 gene in rice, encoding an ARM repeat protein, reveals its pivotal role in regulating PCD and innate immune responses independently of pathogen attack.
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ISSN:1939-8425
1939-8433
1934-8037
DOI:10.1186/s12284-024-00731-x