The Salt-Overly-Sensitive (SOS) signaling module, comprising the sodium-transport protein SOS1 and the regulatory proteins SOS2 and SOS3, is well known as the central salt excretion system, which helps protect plants against salt stress. Here we report that VPS23A, a component of the ESCRT (endosomal sorting complex required for transport), plays an essential role in the function of the SOS module in conferring plant salt tolerance. VPS23A enhances the interaction of SOS2 and SOS3. In the presence of salt stress, VPS23A positively regulates the redistribution of SOS2 to the plasma membrane, which then activates the antiporter activity of SOS1 to reduce Na⁺ accumulation in plant cells. Genetic evidence demonstrated that plant salt tolerance achieved by the overexpression of SOS2 and SOS3 dependeds on VPS23A. Taken together, our results revealed that VPS23A is a crucial regulator of the SOS module and affects the localization of SOS2 to the cell membrane. Moreover, the strong salt tolerance of Arabidopsis seedlings conferred by the engineered membrane-bound SOS2 revealed the significance of SOS2 sorting to the cell membrane in achieving its function, providing a potential strategy for crop salt tolerance engineering.

盐分过度敏感（SOS）信号模块，包括钠转运蛋白SOS1和调节蛋白SOS2和SOS3，众所周知是中央盐分排泄系统，它有助于保护植物免受盐胁迫。在这里我们报告说，VPS23A是ESCRT（运输所需的内体分拣复合体）的组成部分，在赋予植物耐盐性的SOS模块功能中起着至关重要的作用。VPS23A增强了SOS2和SOS3的交互。在存在盐胁迫的情况下，VPS23A积极调节SOS2向质膜的重新分布，然后激活SOS1的反转运蛋白活性以减少植物细胞中的Na ⁺积累。遗传证据表明，SOS2和SSO2的过表达可达到植物对盐的耐受性SOS3取决于VPS23A。两者合计，我们的结果表明VPS23A是SOS模块的关键调节剂，并影响SOS2在细胞膜上的定位。此外，工程化的膜结合SOS2赋予拟南芥幼苗较强的耐盐性，这揭示了将SOS2分选到细胞膜上对实现其功能的重要性，为作物耐盐性工程提供了潜在的策略。