类受体酪氨酸激酶STRK1调控水稻耐盐性的分子机制

Studying on the tolerance to salt stress and breeding new varieties with higher tolerance to salt stress in rice are of great significance for improving grain production and ensuring food safety in China. Our previous studies found that a novel receptor-like cytoplasmic kinase STRK1 could phosphorylate CatC at Tyr210 to positively regulate the salt tolerance in rice, and STRK1 is the only kinase that has been found so far to phosphorylate the tyrosine residues of CAT. Whereas, the pathway and molecular mechanism of salt signal transduction mediated by STRK1 remain to be elucidated. Accordingly, the following main researches will be carried out in this project: (1) Screening and identification of RLK that can interact with STRK1 to illustrate the mechanism of salt signal transmembrane transduction; (2) Identification of the key phospho-tyrosine sites at the RLK-STRK1-CATs pathway to elucidate the characteristics and roles of tyrosine phosphorylation cascade in salt stress signal transduction pathway; (3) Identification and evaluation the allele variations of RLK, STRK1 and CATs as the backbone members of signal transduction, and analysis of their potential application values. The aims of this project are to establish a complete signal transduction pathway of RLK-STRK1-CATs, to reveal the fine molecular mechanism of salt signal transduction mediated by STRK1, and to provide theoretical guidance and characteristic molecular markers of salt tolerance for breeding of salt tolerant crop varieties.

水稻耐盐性研究及耐盐品种选育对提高我国粮食产量、保障粮食安全意义重大。我们前期研究发现一个新的类受体胞质激酶STRK1能磷酸化CatC的Tyr210而正调控水稻耐盐性，且STRK1是迄今发现唯一能磷酸化CAT的酪氨酸残基的激酶，但其介导的盐胁迫信号转导通路与分子机制仍有待阐明。据此，课题拟开展以下主要研究：(1) 筛选鉴定与STRK1互作的RLK，解析其介导的盐胁迫信号跨膜转导机制；(2) 鉴定RLK-STRK1-CATs通路中关键酪氨酸磷酸化位点，阐明酪氨酸级联磷酸化特性及其在信号转导通路中的作用；(3) 鉴定和评价信号转导骨干成员RLK、STRK1和CATs的等位变异，分析其在耐盐品种培育中的应用价值。本项目旨在确立RLK-STRK1-CATs的信号转导完整通路，解析STRK1介导的盐胁迫信号转导的精细分子机制，为水稻耐盐品种的选育提供理论指导和耐盐的特征性分子标记。

水稻耐盐性研究及耐盐品种选育对提高我国粮食产量、保障粮食安全意义重大。我们以前期研究发现的类受体胞质激酶STRK1磷酸化CatC的盐胁迫信号转导通路为基础，解析了翻译后修饰（如磷酸化和S-酰化）参与盐胁迫响应调控的分子机制。项目取得了一下主要研究结果：(1) STRK1磷酸化CatC的Tyr210还参与了CatC稳定性的调控； (2) 发现在STRK1和CATs间存在酪氨酸级联磷酸化的信号转导机制； (3) 鉴定了一个在过氧化物酶体中将CatC的Ser-9去磷酸化的磷酸酶PC1，负调控水稻耐盐性；(4) 发掘和鉴定了一个CatC的等位变异noe1-2，发现其PTS1缺失导致无法定位于过氧化物酶体而发挥功能；(5) 构建了OsDHHC cDNA文库，并解析了STRK1的S-酰化修饰参与盐胁迫响应调控的分子机制；(6) 发掘和鉴定了多个能提高水稻氮同化效率、耐旱性和耐碱性的真菌NADP(H)型GDH基因；(7) 共发表论文11篇，其中4篇为SCI论文（1篇为专业Top期刊The Plant Journal），参与出版专著1部，授权国家发明专利3项，申请国家发明专利2项。本项目解析了STRK1介导的盐胁迫信号转导的精细分子机制，为水稻耐盐品种的选育提供理论指导和耐盐的特征性分子标记。