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题目：钙信号和植物耐盐碱机制

报告人:郭岩

Time：4月19日下午2:00

Room：理科楼430

Abstract：

The Salt Overly Sensitive (SOS) pathway regulates intracellular sodium ion (Na+) homeostasis and salt tolerance in plants. In this pathway, a salt stress-induced transient increase in cytosolic calcium activates two calcium sensors, SOS3 and SOS3-Like Calcium Binding Protein8, which interact with and activate the SOS2 protein kinase. The SOS3/SCaBP8-SOS2 complex then activates SOS1, a plasma membrane Na+/H+ antiporter which transports sodium from the cytosol. So far, the mechanisms that control inhibition of the SOS pathway when plants are grown in the absence of salt stress have remained elusive. We demonstrate that the λ and κ 14-3-3 proteins interact with SOS2 and repress its kinase activity. 14-3-3 λ interacts with the SOS2 junction domain, which has previously been shown to be important for its kinase activity. A phosphorylation site (Ser294) was identified within this domain by mass spectrometry. Mutation of Ser294 to Alanine (A) or Aspartate (D) did not affect SOS2 kinase activity in the absence of 14-3-3s. However, the S/A mutation decreased the 14-3-3-dependent inhibition of activity, while the S/D mutation increased this inhibitory effect. SOS2S294A rescued the salt-sensitive phenotype of the sos2-2 mutant to wild-type levels while SOS2S294D did not. Moreover, we find that anther protein kinase phosphorylates the SOS2 Ser294 site in normal condition. Upon salt stress, this kinase activity is repressed by the 14-3-3 proteins, which in turn releases the SOS2 activity for activating SOS1. These results identify 14-3-3 proteins as important regulators of salt tolerance and uncover their role in a mechanism that confers basal repression of the SOS pathway in the absence of salt stress. 

报告人简介:

中国农业大学生物学院教授

国家杰出青年基金获得者、特聘教授, 973项目首席科学家,入选国家百千万人才工程。在Developmental Cell, PNAS, Plant Cell等刊物发表几十篇论文.