GSK3类蛋白激酶SGK1通过SOS2调节植物耐盐性的分子机制研究

土壤盐碱化严重影响作物生长与农业生产，对我国粮食安全造成重大危害。理解植物响应盐胁迫的分子机制，可以为改良作物、提高作物的耐盐能力等提供重要的科学依据。Salt-Overly-Sensitive（SOS）信号途径是参与调节植物耐盐性的重要通路，对于维持盐胁迫条件下植物细胞内的离子平衡具有重要作用。SOS信号通路可被盐胁迫激活以提高植物的耐盐性，但尚未发现参与在盐胁迫条件下激活其关键组分SOS2的上游激酶。本项目前期工作发现一类GSK3类蛋白激酶SGK1可与SOS2互作；SGK1可被盐胁迫激活并磷酸化修饰SOS2，从而激活SOS2；SGK1功能缺失突变体对盐胁迫耐受能力降低。本项目拟继续深入研究SGK1通过调节SOS2的激酶活性而调节植物耐盐性的分子机制，并分析BR信号通路对植物响应盐胁迫信号转导过程的调控作用，上述工作将有助于加深人们对SOS信号通路以及植物耐盐性的认识。

Soil salinity is a widespread abiotic stress with significant agricultural impact, which reduces plant growth and crop productivity. Understanding the mechanism of plant salt tolerance provides the possibility for crop engineering to enhance its tolerance to salt stress. Salt-Overly-Sensitive (SOS) signaling pathway regulates potassium and sodium ion homeostasis in plant cell during salt stress. Although numerous studies have revealed how components of SOS signaling pathway are regulated in response to salt stress, some key questions still need to be answered. Our previous data indicate that a GSK3-like protein kinase SGK1 interacts with SOS2. SGK1 can be activated by salt stress and phosphorylates/activates SOS2, leading to the full activation of SOS pathway to enhance plant salt tolerance during salt stress. We will further study the mechanism by which SGK1 regulates salt tolerance through SOS2 and the regulatory role of BR on salt tolerance in plant. Our study provides a new understanding of SOS pathway and salt tolerance.