Lu Kai-Kai, Yang Hong, Liao Cai-Yi, Song Ru-Feng, Hu Xiao-Yu, Ren Feng, Liu Wen-Cheng
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; Key Laboratory of Pesticide and Chemical Biology of Ministry of Education, Hubei Key Laboratory of Genetic Regulation and Integrative Biology, School of Life Sciences, Central China Normal University, Wuhan 430079, China.
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; The Zhongzhou Laboratory for Integrative Biology, Henan University, Zhengzhou, Henan 450000, China; Sanya Institute, Henan University, Sanya 572025, China.
Dev Cell. 2025 Jun 6. doi: 10.1016/j.devcel.2025.05.010.
Salt stress impacts plant growth and development, threatening agricultural production. The Na/H antiporter SALT OVERLY SENSITIVE 1 (SOS1) functions in cellular ion homeostasis through facilitating Na excretion and is therefore essential for plant salt tolerance. Here, we report that the transcription factors AUXIN RESPONSE FACTOR 7 (ARF7) and ARF19 are required for salt-induced SOS1 expression and salt tolerance in Arabidopsis thaliana. ARF7 and ARF19 activate SOS1 transcription by binding to SOS1 coding region rather than its promoter. Additionally, an E3 ubiquitin ligase, CHY ZINC-FINGER AND RING PROTEIN 1 (CHYR1), interacts with and degrades ARF7 and ARF19, dampening SOS1 expression. Upon high salinity, CHYR1 expression is inhibited in plants, stabilizing ARF7 and ARF19 proteins and increasing SOS1 expression. Collectively, our study identifies a transcriptional cis-element within SOS1 coding region recognized by ARF7 and ARF19 and elucidates a molecular mechanism governing ARF7 and ARF19 protein stability and SOS1 expression during plant salt stress response.
盐胁迫影响植物的生长发育，威胁着农业生产。钠/氢逆向转运蛋白盐过度敏感1（SOS1）通过促进钠的排出在细胞离子稳态中发挥作用，因此对植物耐盐性至关重要。在此，我们报道转录因子生长素响应因子7（ARF7）和ARF19是拟南芥中盐诱导的SOS1表达和耐盐性所必需的。ARF7和ARF19通过结合SOS1编码区而非其启动子来激活SOS1转录。此外，一种E3泛素连接酶，CHY锌指和环蛋白1（CHYR1），与ARF7和ARF19相互作用并使其降解，从而抑制SOS1表达。在高盐度条件下，植物中CHYR1的表达受到抑制，使ARF7和ARF19蛋白稳定并增加SOS1表达。总之，我们的研究确定了SOS1编码区内被ARF7和ARF19识别的转录顺式元件，并阐明了植物盐胁迫响应过程中控制ARF7和ARF19蛋白稳定性及SOS1表达的分子机制。
