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持绿基因(OsSGR)的自然突变通过提高细胞分裂素含量赋予水稻对纹枯病更强的抗性。

Natural mutation in Stay-Green (OsSGR) confers enhanced resistance to rice sheath blight through elevating cytokinin content.

作者信息

Xie Wenya, Xue Xiang, Wang Yu, Zhang Guiyun, Zhao Jianhua, Zhang Huimin, Wang Guangda, Li Lei, Wang Yiqin, Shan Wenfeng, Zhang Yafang, Chen Zongxiang, Chen Xijun, Feng Zhiming, Hu Keming, Sun Mingfa, Chu Chengcai, Zuo Shimin

机构信息

Jiangsu Key Laboratory of Crop Genomics and Molecular Breeding/Zhongshan Biological Breeding Laboratory/Key Laboratory of Plant Functional Genomics of the Ministry of Education, Agricultural College of Yangzhou University, Yangzhou, China.

Jiangsu Co-Innovation Center for Modern Production Technology of Grain Crops/Jiangsu Key Laboratory of Crop Genetics and Physiology, Yangzhou University, Yangzhou, China.

出版信息

Plant Biotechnol J. 2025 Mar;23(3):807-823. doi: 10.1111/pbi.14540. Epub 2024 Dec 4.

DOI:10.1111/pbi.14540
PMID:39630094
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11869175/
Abstract

Sheath blight (ShB), caused by Rhizoctonia solani, is a highly destructive disease in many crops worldwide and no major resistance genes are available. Here, we identified a sbr1 (sheath blight resistance 1) rice mutant, which shows enhanced ShB resistance and maintains wildtype agronomic traits including yield, but carries an undesired stay-green phenotype. Through map-based cloning and transgenic validation, we found that an insertion disrupting the Stay-Green (OsSGR) gene is responsible for sbr1 phenotypes. Mechanistically, the sbr1/Ossgr mutants reduce the expression of most OsCKX genes, which function in cytokinin (CK) degradation, to accumulate CK leading to ShB resistance. Importantly, knockout of OsCKX7, predominantly expressed in the leaf sheath and highly induced by R. solani, significantly enhances ShB resistance without stay-green phenotype nor yield penalty, showing high application potential. Thus, our study reveals novel insights that OsSGR and cytokinin play key roles in rice-R. solani interaction and generates a valuable ShB-resistant germplasm.

摘要

纹枯病(ShB)由立枯丝核菌引起,是全球许多作物中极具破坏性的病害,目前尚无主要抗性基因。在此,我们鉴定出一个sbr1(纹枯病抗性1)水稻突变体,其对纹枯病的抗性增强,且保持包括产量在内的野生型农艺性状,但具有不理想的持绿表型。通过图位克隆和转基因验证,我们发现一个破坏持绿基因(OsSGR)的插入导致了sbr1的表型。从机制上讲,sbr1/OsSGR突变体降低了大多数在细胞分裂素(CK)降解中起作用的OsCKX基因的表达,从而积累CK导致对纹枯病产生抗性。重要的是,在叶鞘中主要表达且受立枯丝核菌高度诱导的OsCKX7基因敲除,显著增强了对纹枯病的抗性,且没有持绿表型也不影响产量,显示出很高的应用潜力。因此,我们的研究揭示了新的见解,即OsSGR和细胞分裂素在水稻与立枯丝核菌的相互作用中起关键作用,并产生了一种有价值的抗纹枯病种质。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/19f7/11869175/b465bea726cb/PBI-23-807-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/19f7/11869175/42070f4b53ca/PBI-23-807-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/19f7/11869175/ba88953ef06d/PBI-23-807-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/19f7/11869175/89456d317120/PBI-23-807-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/19f7/11869175/a7acd67a7cbf/PBI-23-807-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/19f7/11869175/caefd68e7327/PBI-23-807-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/19f7/11869175/3b5ff66c83d9/PBI-23-807-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/19f7/11869175/ba9610cc421c/PBI-23-807-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/19f7/11869175/28ab98e78b87/PBI-23-807-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/19f7/11869175/b465bea726cb/PBI-23-807-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/19f7/11869175/42070f4b53ca/PBI-23-807-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/19f7/11869175/ba88953ef06d/PBI-23-807-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/19f7/11869175/89456d317120/PBI-23-807-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/19f7/11869175/a7acd67a7cbf/PBI-23-807-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/19f7/11869175/caefd68e7327/PBI-23-807-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/19f7/11869175/3b5ff66c83d9/PBI-23-807-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/19f7/11869175/ba9610cc421c/PBI-23-807-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/19f7/11869175/28ab98e78b87/PBI-23-807-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/19f7/11869175/b465bea726cb/PBI-23-807-g008.jpg

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