{"title":"Natural variation in SBRR1 shows high potential for sheath blight resistance breeding in rice","authors":"Zhiming Feng, Peng Gao, Guangda Wang, Houxiang Kang, Jianhua Zhao, Wenya Xie, Rujia Chen, Ran Ju, Xuli Wang, Zhaogen Wei, Huimin Zhang, Jinqiao Zhang, Yafang Zhang, Keming Hu, Quanyi Sun, Yuntao Zhu, Yehui Xiong, Xi Liu, Xijun Chen, Zongxiang Chen, Chao Yang, Jun Liu, Guo-Liang Wang, Sheng-Wei Zhang, Zefeng Yang, Shimin Zuo","doi":"10.1038/s41588-025-02281-4","DOIUrl":null,"url":null,"abstract":"Sheath blight (ShB), caused by necrotrophic fungus Rhizoctonia solani, is one of the most serious rice diseases worldwide. To the best of our knowledge, no genes with high potential for rice ShB resistance breeding have been previously characterized. Here we identify a ShB resistance receptor-like kinase 1 (SBRR1) gene via a genome-wide association study. The SBRR1-R elite allele, containing a 256-bp insertion in its promoter, is preferentially present in indica varieties in geographical regions with highly favorable conditions for ShB development. Introduction of SBRR1-R into a commercial japonica rice variety significantly reduces yield loss under severe ShB disease pressure. Transcription factor bHLH57 specifically binds to the 256-bp sequence and accounts for highly induced expression and stronger resistance of SBRR1-R. Localization of SBRR1 on plasma membrane, aided by SBRR1-interaction-protein 1, and phosphorylation of SBRR1 are required for SBRR1 to rapidly upregulate downstream chitinase genes for resistance. These findings offer mechanistical insights into ShB resistance hidden in natural rice varieties. A genome-wide association study in rice identifies variation in SBRR1 associated with sheath blight resistance. Introducing the SBRR1-R allele into a commercial rice variety reduces yield loss under severe exposure to sheath blight disease.","PeriodicalId":18985,"journal":{"name":"Nature genetics","volume":"57 8","pages":"2004-2016"},"PeriodicalIF":29.0000,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41588-025-02281-4.pdf","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Nature genetics","FirstCategoryId":"99","ListUrlMain":"https://www.nature.com/articles/s41588-025-02281-4","RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"GENETICS & HEREDITY","Score":null,"Total":0}
引用次数: 0
Abstract
Sheath blight (ShB), caused by necrotrophic fungus Rhizoctonia solani, is one of the most serious rice diseases worldwide. To the best of our knowledge, no genes with high potential for rice ShB resistance breeding have been previously characterized. Here we identify a ShB resistance receptor-like kinase 1 (SBRR1) gene via a genome-wide association study. The SBRR1-R elite allele, containing a 256-bp insertion in its promoter, is preferentially present in indica varieties in geographical regions with highly favorable conditions for ShB development. Introduction of SBRR1-R into a commercial japonica rice variety significantly reduces yield loss under severe ShB disease pressure. Transcription factor bHLH57 specifically binds to the 256-bp sequence and accounts for highly induced expression and stronger resistance of SBRR1-R. Localization of SBRR1 on plasma membrane, aided by SBRR1-interaction-protein 1, and phosphorylation of SBRR1 are required for SBRR1 to rapidly upregulate downstream chitinase genes for resistance. These findings offer mechanistical insights into ShB resistance hidden in natural rice varieties. A genome-wide association study in rice identifies variation in SBRR1 associated with sheath blight resistance. Introducing the SBRR1-R allele into a commercial rice variety reduces yield loss under severe exposure to sheath blight disease.
期刊介绍:
Nature Genetics publishes the very highest quality research in genetics. It encompasses genetic and functional genomic studies on human and plant traits and on other model organisms. Current emphasis is on the genetic basis for common and complex diseases and on the functional mechanism, architecture and evolution of gene networks, studied by experimental perturbation.
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