Abstract：
High salinity stress promotes plant ethylene biosynthesis and triggers the ethylene signalling response. However, the precise mechanism underlying how plants transduce ethylene signalling in response to salt stress remains largely unknown. In this study, we discovered that SALT OVERLY SENSITIVE 2 (SOS2) inhibits the kinase activity of CONSTITUTIVE TRIPLE RESPONSE1 (CTR1) by phosphorylating the 87th serine (S87). This phosphorylation event activates the ethylene signalling response, leading to enhanced plant salt resistance. Furthermore, through genetic analysis, we determined that the loss of CTR1 or the gain of SOS2-mediated CTR1 phosphorylation both contribute to improved plant salt tolerance. Additionally, in the sos2 mutant, we observed compromised proteolytic processing of ETHYLENE INSENSITIVE 2 (EIN2) and reduced nuclear localization of EIN2 C-terminal fragments (EIN2-C), which correlate with decreased accumulation of ETHYLENE INSENSITIVE 3 (EIN3). Collectively, our findings unveil the role of the SOS2-CTR1 regulatory module in promoting the activation of the ethylene signalling pathway and enhancing plant salt tolerance.
摘要：
高盐度胁迫促进植物乙烯生物合成并触发乙烯信号应答。然而,植物如何转导乙烯信号以响应盐胁迫的确切机制仍然未知。在这项研究中,我们发现盐过度敏感2（SOS2）通过磷酸化第87丝氨酸（S87）抑制本构三反应1（CTR1）的激酶活性。这个磷酸化事件激活了乙烯信号应答,导致植物耐盐性增强。此外，通过基因分析,我们确定CTR1的丢失或SOS2介导的CTR1磷酸化的增加都有助于提高植物的耐盐性。此外,在sos2突变体中，我们观察到乙烯不敏感2（EIN2）的蛋白水解过程受损和EIN2C末端片段（EIN2-C）的核定位减少，这与乙烯不敏感3（EIN3）的积累减少有关。总的来说，我们的发现揭示了SOS2-CTR1调控模块在促进乙烯信号通路激活和增强植物耐盐性方面的作用.
