类受体激酶GSO1响应盐胁迫的分子机制研究

盐胁迫是限制农作物生产的重要环境因素。类受体激酶是一类在感受、传递环境信号方面起重要作用的蛋白激酶，但是，关于类受体激酶参与盐胁迫信号转导方面的报道较少。我们通过对拟南芥类受体激酶T-DNA插入突变体库盐表型筛选，发现一个盐敏感的突变体gso1。GSO1回补株系完全恢复gso1的盐表型。为了研究GSO1参与盐胁迫响应的分子机制，我们通过免疫共沉淀串联质谱发现SOS2与GSO1互作。磷酸化实验显示，GSO1磷酸化SOS2。gso1中SOS2的激酶活性降低。MST实验发现，GSO1的胞外域与Na+结合。并且，盐胁迫下SOS2进入细胞核。gso1中一些盐诱导基因的表达下降。我们推测，盐胁迫下GSO1可能感受胞外Na+，其胞内激酶结构域磷酸化并激活SOS2，进而调控SOS2参与的盐胁迫信号转导。因此，我们拟通过生理、生化和遗传等手段，开展相关的实验，以期阐明GSO1响应盐胁迫的分子机制。

Salt stress is an important environmental factor restricting crop production. Receptor-like kinases are a class of protein kinases that play an important role in sensing and transmitting environmental signals. However, there are few reports about receptor-like kinases involved in salt stress signal transduction. We screened the salt phenotype of the Arabidopsis receptor kinase T-DNA insertion mutant library and found a salt-sensitive mutant gso1. The GSO1 complementary line completely restored the salt phenotype of gso1. In order to study the molecular mechanism of GSO1 participating in response to salt stress, we found a candidate protein SOS2 that interacts with GSO1 by co-immunoprecipitation and mass spectrometry. Phosphorylation experiments showed that GSO1 phosphorylates SOS2. The kinase activity of SOS2 is reduced in gso1. MST experiments found that the extracellular domain of GSO1 binds to Na+. Moreover, SOS2 enters the nucleus under salt stress. The expression of some salt-induced genes in gso1 decreased. We speculate that GSO1 may sense extracellular Na+ under salt stress, and its intracellular kinase domain phosphorylates and activates SOS2, which in turn regulates the salt stress signaling involved in SOS2. Therefore, we intend to carry out relevant experiments through physiological, biochemical and genetic means, in order to clarify the molecular mechanism of GSO1 response to salt stress.