A key mechanism employed by plants to adapt to salinity stress involves maintaining ion homeostasis via the actions of ion transporters. While the function of cation transporters in maintaining ion homeostasis in plants has been extensively studied, little is known about the roles of their anion counterparts in this process. Here, we describe a mechanism of salt adaptation in plants. We characterized the chloride channel (CLC) gene AtCLCf, whose expression is regulated by WRKY transcription factor under salt stress in Arabidopsis thaliana. Loss-of-function atclcf seedlings show increased sensitivity to salt, whereas AtCLCf overexpression confers enhanced resistance to salt stress. Salt stress induces the translocation of GFP-AtCLCf fusion protein to the plasma membrane (PM). Blocking AtCLCf translocation using the exocytosis inhibitor brefeldin-A or mutating the small GTPase gene AtRABA1b/BEX5 (RAS GENES FROM RAT BRAINA1b homolog) increases salt sensitivity in plants. Electrophysiology and liposome-based assays confirm the Cl⁻/H⁺ antiport function of AtCLCf. Therefore, we have uncovered a mechanism of plant adaptation to salt stress involving the NaCl-induced translocation of AtCLCf to the PM, thus facilitating Cl⁻ removal at the roots, and increasing the plant’s salinity tolerance.

植物适应盐度胁迫的关键机制涉及通过离子转运蛋白的作用维持离子稳态。虽然阳离子转运蛋白在维持植物离子稳态中的功能已被广泛研究，但对其阴离子对应物在此过程中的作用知之甚少。在这里，我们描述了植物的盐适应机制。我们对拟南芥氯离子通道( CLC )基因AtCLCf进行了表征，该基因在盐胁迫下的表达受WRKY转录因子的调控。功能丧失的atclcf幼苗表现出对盐的敏感性增加，而AtCLCf过度表达则增强了对盐胁迫的抵抗力。盐胁迫诱导 GFP-AtCLCf 融合蛋白易位至质膜 (PM)。使用胞吐抑制剂 brefeldin-A 阻断 AtCLCf 易位或突变小 GTPase 基因AtRABA1b/BEX5（来自 RAT BRAINA1b同源物的 RAS 基因）可增加植物的盐敏感性。电生理学和基于脂质体的测定证实了AtCLCf 的Cl ^- /H ⁺反向转运功能。因此，我们发现了植物适应盐胁迫的机制，涉及氯化钠诱导的AtCLCf向PM的易位，从而促进根部Cl ^{- 的去除，并提高植物的耐盐性。}