维持细胞内的离子平衡是植物适应盐胁迫的重要机制。研究发现盐胁迫下质膜H+-ATPase和Na+/H+antiporter活性被协同调控来维持植物细胞离子的稳定，但协同调控机制尚不清楚。已有工作表明正常条件下14-3-3λ与Ser-294被磷酸化的SOS2结合，抑制SOS2活性，负调控SOS （Salt Overly Sensitive）途径，但不清楚磷酸化修饰SOS2 Ser-294的蛋白。我们发现PKS5磷酸化修饰SOS2 Ser-294位点。另外发现14-3-3λ抑制PKS5激酶活性，在盐胁迫下正调控H+-ATPase活性。表明14-3-3λ可能为盐胁迫下调控H+-ATPase和Na+/H+ antiporter活性的偶联因子。因此，本申请将研究14-3-3λ在盐胁迫过程中调控H+-ATPase和Na+/H+ antiporter活性的“桥梁”作用，深入阐明植物适应盐胁迫的分子机制。

The maintenance of intracellular ionic homeostasis is an important mechanism of plants in response to salt stress. To avoid accumulation of toxic Na+ ion in cytosal, the activities of plasma membrane (PM) H+-ATPase and Na+/H+ antiporter are regulated synergistically under salt stress in plant cells, however, the mechanism of co-regulating the two enzymic activities is elusive. Previous study has found that 14-3-3 λ interacts with SOS2 at the phosphorylated Ser-294 and represses SOS2 kinase activity to inhibit SOS1 activity, a Na+/H+ antiporter, when plants grow in the absence of salt stress, but protein for phosphoralation of the SOS2 Ser-294 is undefinable. We find that PKS5 kinase, a negative regulator of PM H+-ATPase, phosphoraltes the SOS2 S-294, and the 14-3-3 λ represses the PKS5 kinase activity and positively regulates the PM H+-ATPase activity under salt stress. These results indicate that 14-3-3 λ is an important regulator in mediating the activities of PM H+-ATPase and Na+/H+ antiporter coordinately under salt stress. In this study, we will analyze the detail function of 14-3-3 λ in co-regulating the activities of PM H+-ATPase and Na+/H+ antiporter, and to clarify the mechanism of plant in response to salt stress.