Na+/H+逆转运蛋白GmSOS1自抑制域调控大豆耐盐性的研究

Na+/H+逆转运蛋白SOS1是将细胞质中的Na+运输到胞外的SOS途径中的重要蛋白质，其自抑制域对调控SOS1蛋白质活性起关键作用。项目组前期利用CRISPR/Cas9技术，编辑大豆GmSOS1激活域和自抑制域的连接序列，获得了GmSOS1自抑制域突变体Gmsos1-3和Gmsos1-4。在NaCl胁迫条件下，与野生型Willams82相比，突变体表现出明显的耐盐性。我们推测自抑制域突变使GmSOS1保持组成型的活化状态，从而提高了植株外排Na+的能力。项目将以GmSOS1自抑制域突变体为试材，从GmSOS1蛋白的转运活性，GmSOS1蛋白质的表达水平、磷酸化程度及同源二聚化情况，相互作用蛋白等方面，深入研究大豆GmSOS1自抑制域在调节GmSOS1活性中的具体功能及与植物的耐盐性之间的相关关系，揭示GmSOS1响应盐胁迫反应的分子机制，同时为大豆耐盐的分子育种提供理论基础。

The plasma membrane sodium/proton exchanger Salt-Overly-Sensitive 1 (SOS1) is a critical determinant to efflux Na+. Autoinhibitory domain of SOS1 protein plays an important role in regulating the activity of SOS1 protein. We have obtained salt tolerance gmsos1 mutants in soybean by editing the linker of activation domain and autoinhibitory domain using CRISPR/Cas9 system. Mutants Gmsos1-3 and Gmsos1-4 showed salt tolerance under NaCl treatment. We hypnosis that mutation in autoinhibitory domain of GmSOS1 will keep constitutive activation of GmSOS1 to improve the ability to efflux Na+. Furthermore, we will perform experiments to detect gene expression pattern, the transfer activity, phosphorylation and dimerization of GmSOS1 protein under NaCl stress condition, screen the interactive proteins of GmSOS1 protein in mutants. The results will give us new understanding how GmSOS1 autoinhibitory domain regulate GmSOS1 and relationship with salt tolerance which can enrich the function and molecular mechanism of SOS1 and provide support of application in molecular breeding of salt tolerance soybean .