Calcium-activated 14-3-3 proteins as a molecular switch in salt stress tolerance

• 全文链接

钙激活的14-3-3蛋白作为盐胁迫耐受的分子开关

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来源：

Nature Communications

全文链接：

//agri.nais.net.cn/topic/downloadFile/7367a4f1-7792-4392-8ad8-1ea201c8b880

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资源所属：

种质资源保护与创制专题

类型：

学术文献

语种：

英语

原文发布日期：

2019-03-13

摘要：

Calcium is a universal secondary messenger that triggers many cellular responses. However, it is unclear how a calcium signal is coordinately decoded by different calcium sensors, which in turn regulate downstream targets to fulfill a specific physiological function. Here we show that SOS2-LIKE PROTEIN KINASE5 (PKS5) can negatively regulate the Salt-Overly-Sensitive signaling pathway in Arabidopsis. PKS5 can interact with and phosphorylate SOS2 at Ser294, promote the interaction between SOS2 and 14-3-3 proteins, and repress SOS2 activity. However, salt stress promotes an interaction between 14-3-3 proteins and PKS5, repressing its kinase activity and releasing inhibition of SOS2. We provide evidence that 14-3-3 proteins bind to Ca2+, and that Ca2+ modulates 14-3-3-dependent regulation of SOS2 and PKS5 kinase activity. Our results suggest that a salt-induced calcium signal is decoded by 14-3-3 and SOS3/SCaBP8 proteins, which selectively activate/inactivate the downstream protein kinases SOS2 and PKS5 to regulate Na+ homeostasis by coordinately mediating plasma membrane Na+/H+ antiporter and H+-ATPase activity.