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FKBP12-EBP1介导的水稻耐盐性调控

FKBP12-EBP1-Mediated Regulation of Salinity Tolerance in Rice.

作者信息

Jiang Yaohuang, Wang Mingyang, Wu Limin, Dong Guojun, Chen Fei, Zhang Yanli, Qian Qian, Ruan Banbu, Yu Yanchun

机构信息

College of Life and Environmental Sciences, Hangzhou Normal University, Hangzhou, China.

State Key Laboratory of Rice Biology and Breeding, China National Rice Research Institute, Hangzhou, Zhejiang, China.

出版信息

Plant Cell Environ. 2025 Aug;48(8):6285-6300. doi: 10.1111/pce.15583. Epub 2025 May 8.

Abstract

Salt stress poses a significant threat to rice productivity and global food security. This study investigates the role of EBP1, a homolog of ErbB3 Binding Protein 1, in regulating salt tolerance in rice. We found that salt treatment induces OsEBP1 expression. Functional analyses reveal that overexpression of OsEBP1 enhances salt tolerance in rice, while knockout mutants show reduced salt tolerance. In the ebp1-1 mutant, salt stress leads to the downregulation of key ion homeostasis genes, including HKT1;1, SOS1, and HAK1, resulting in elevated Na levels and disrupted Na/K⁺ balance. Additionally, OsEBP1 overexpression lines exhibit enhanced antioxidant defenses, characterized by reduced reactive oxygen species (ROS) accumulation and increased activity of antioxidant enzymes, such as APX, CAT, and POD. Further investigation reveals that EBP1 directly interacts with FKBP12, which promotes EBP1 degradation via the 26S proteasome pathway. Genetic analysis indicates that FKBP12 acts as a negative regulator of EBP1, and its downregulation stabilizes EBP1 levels under salt stress, thereby enhancing salt tolerance. In conclusion, these findings provide novel insights into the molecular mechanism underlying the FKBP12-EBP1 interaction in salt stress tolerance, providing a basis for developing salt-tolerant rice cultivars to bolster sustainable agriculture in salinity-affected regions.

摘要

盐胁迫对水稻产量和全球粮食安全构成重大威胁。本研究调查了ErbB3结合蛋白1的同源物EBP1在调节水稻耐盐性中的作用。我们发现盐处理可诱导OsEBP1表达。功能分析表明,OsEBP1过表达增强了水稻的耐盐性,而敲除突变体的耐盐性降低。在ebp1-1突变体中,盐胁迫导致关键离子稳态基因(包括HKT1;1、SOS1和HAK1)的下调,导致Na水平升高和Na/K⁺平衡破坏。此外,OsEBP1过表达系表现出增强的抗氧化防御能力,其特征是活性氧(ROS)积累减少,抗氧化酶(如APX、CAT和POD)的活性增加。进一步研究表明,EBP1直接与FKBP12相互作用,FKBP12通过26S蛋白酶体途径促进EBP1降解。遗传分析表明,FKBP12作为EBP1的负调节因子,其下调可在盐胁迫下稳定EBP1水平,从而增强耐盐性。总之,这些发现为盐胁迫耐受性中FKBP12-EBP1相互作用的分子机制提供了新的见解,为培育耐盐水稻品种以促进盐渍化地区的可持续农业提供了依据。

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