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CycC1;1-WRKY75 复合物介导的 SOS1 转录调控控制拟南芥的耐盐性。

CycC1;1-WRKY75 complex-mediated transcriptional regulation of SOS1 controls salt stress tolerance in Arabidopsis.

机构信息

State Key Laboratory of Crop Stress Adaptation and Improvement, Collaborative Innovation Center of Crop Stress Biology, College of Life Sciences, Henan University, Kaifeng 475004, China.

Hubei Key Laboratory of Genetic Regulation and Integrative Biology, School of Life Sciences, Central China Normal University, Wuhan 430079, China.

出版信息

Plant Cell. 2023 Jun 26;35(7):2570-2591. doi: 10.1093/plcell/koad105.

Abstract

SALT OVERLY SENSITIVE1 (SOS1) is a key component of plant salt tolerance. However, how SOS1 transcription is dynamically regulated in plant response to different salinity conditions remains elusive. Here, we report that C-type Cyclin1;1 (CycC1;1) negatively regulates salt tolerance by interfering with WRKY75-mediated transcriptional activation of SOS1 in Arabidopsis (Arabidopsis thaliana). Disruption of CycC1;1 promotes SOS1 expression and salt tolerance in Arabidopsis because CycC1;1 interferes with RNA polymerase II recruitment by occupying the SOS1 promoter. Enhanced salt tolerance of the cycc1;1 mutant was completely compromised by an SOS1 mutation. Moreover, CycC1;1 physically interacts with the transcription factor WRKY75, which can bind to the SOS1 promoter and activate SOS1 expression. In contrast to the cycc1;1 mutant, the wrky75 mutant has attenuated SOS1 expression and salt tolerance, whereas overexpression of SOS1 rescues the salt sensitivity of wrky75. Intriguingly, CycC1;1 inhibits WRKY75-mediated transcriptional activation of SOS1 via their interaction. Thus, increased SOS1 expression and salt tolerance in cycc1;1 were abolished by WRKY75 mutation. Our findings demonstrate that CycC1;1 forms a complex with WRKY75 to inactivate SOS1 transcription under low salinity conditions. By contrast, under high salinity conditions, SOS1 transcription and plant salt tolerance are activated at least partially by increased WRKY75 expression but decreased CycC1;1 expression.

摘要

盐过度敏感 1(SOS1)是植物耐盐性的关键组成部分。然而,SOS1 转录在植物响应不同盐度条件下如何动态调节仍不清楚。在这里,我们报告 C 型细胞周期蛋白 1;1(CycC1;1)通过干扰 WRKY75 介导的 SOS1 的转录激活负调控盐胁迫耐受性在拟南芥(Arabidopsis thaliana)中。CycC1;1 的破坏促进了 SOS1 的表达和拟南芥的耐盐性,因为 CycC1;1 通过占据 SOS1 启动子来干扰 RNA 聚合酶 II 的募集。sos1 突变完全削弱了 cycc1;1 突变体的增强耐盐性。此外,CycC1;1 与转录因子 WRKY75 发生物理相互作用,WRKY75 可以结合 SOS1 启动子并激活 SOS1 表达。与 cycc1;1 突变体相反,wrky75 突变体具有减弱的 SOS1 表达和耐盐性,而 SOS1 的过表达挽救了 wrky75 的盐敏感性。有趣的是,CycC1;1 通过它们的相互作用抑制 WRKY75 介导的 SOS1 转录激活。因此,cycc1;1 中 SOS1 表达和耐盐性的增加被 WRKY75 突变所消除。我们的研究结果表明,CycC1;1 在低盐条件下与 WRKY75 形成复合物以失活 SOS1 转录。相比之下,在高盐条件下,SOS1 转录和植物耐盐性至少部分通过增加的 WRKY75 表达和降低的 CycC1;1 表达来激活。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c96/10291036/2a165eeebc76/koad105_ga1.jpg

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