Liu Xiaoxiao, Zhang Lei, Zhao Zeqi, Zheng Yue, Ren Yue, Zhao Xiaomin, Zhang Shizhong, Yang Guodong, Huang Jinguang, Yan Kang, Li Chunlong, Zheng Chengchao, Wu Changai
State Key Laboratory of Wheat Improvement, National Center of Technology Innovation for Comprehensive Utilization of Saline-Alkali Land, Engineering Center of Saline-Alkali Soil Plant-Microbial Joint Restoration, College of Life Sciences, Shandong Agricultural University, Shandong, Tai'an 271018, China.
State Key Laboratory of Wheat Improvement, National Center of Technology Innovation for Comprehensive Utilization of Saline-Alkali Land, Engineering Center of Saline-Alkali Soil Plant-Microbial Joint Restoration, College of Life Sciences, Shandong Agricultural University, Shandong, Tai'an 271018, China; Research Institute for Marine Traditional Chinese Medicine (Qingdao Academy of Chinese Medical Sciences), The SATCM Key Unit of Discovering and Developing New Marine TCM Drugs, Key Laboratory of Marine Traditional Chinese Medicine in Shandong Universities, Shandong University of Traditional Chinese Medicine, Jinan 250355, China.
Cell Rep. 2025 Jun 24;44(6):115729. doi: 10.1016/j.celrep.2025.115729. Epub 2025 May 20.
Although preventing sodium ion import is crucial for salt tolerance, the mechanisms and the Na importers involved remain unclear. We identified NRT1.2/NPF4.6/AIT1 as a non-selective Na importer. NRT1.2 overexpression in Arabidopsis increased salt sensitivity due to Na accumulation, while nrt1.2 mutants exhibited opposite results. Non-invasive micro-test technology indicated Na uptake capability of NRT1.2 in Arabidopsis roots. When expressed in Xenopus laevis oocytes, NRT1.2 displayed low-pH-dependent and NO-promoted Na, K, and Li importer capacity, conferring higher potassium and lithium tolerance in NRT1.2 overexpression plants. Mechanically, salt overly sensitive 2 (SOS2) phosphorylated NRT1.2 at Thr248, reducing its Na import and preventing excessive Na accumulation. Prolonged salt stress also downregulated NRT1.2 transcripts. In summary, our findings unveil a role of NRT1.2 in Na transport and a regulatory pathway via SOS2-mediated phosphorylation of NRT1.2 at Thr248, crucial for plant salt-stress adaptation.
尽管阻止钠离子内流对耐盐性至关重要,但相关机制及涉及的钠离子转运蛋白仍不清楚。我们鉴定出NRT1.2/NPF4.6/AIT1为一种非选择性钠离子转运蛋白。拟南芥中NRT1.2过表达因钠离子积累而增加了盐敏感性,而nrt1.2突变体则表现出相反的结果。非损伤微测技术表明拟南芥根中NRT1.2具有钠离子吸收能力。当在非洲爪蟾卵母细胞中表达时,NRT1.2表现出低pH依赖性且受一氧化氮促进的钠、钾和锂转运蛋白能力,使NRT1.2过表达植物具有更高的钾和锂耐受性。机制上,盐超敏感2(SOS2)在苏氨酸248位点磷酸化NRT1.2,降低其钠离子转运并防止过量钠离子积累。长期盐胁迫也会下调NRT1.2转录本。总之,我们的研究结果揭示了NRT1.2在钠离子转运中的作用以及通过SOS2介导的NRT1.2苏氨酸248位点磷酸化的调控途径,这对植物适应盐胁迫至关重要。