拟南芥MPK3/MPK6介导的细胞壁应答盐胁迫机制研究

环境胁迫是危害农业生产的主要因素，理解植物应答环境胁迫的分子机制是提高作物抗逆性的理论基础。细胞壁是直接与环境条件接触的细胞组分，在植物感知和应答环境胁迫中起重要作用，然而作用机制并不明确。纤维素合酶复合体（CSC）在其结合蛋白CC的帮助下维持盐胁迫下细胞壁中纤维素的合成，是目前阐述最清晰的一种细胞壁应答盐胁迫的作用机制，但CC-CSC如何感知盐胁迫、信号如何传递尚不清楚。已有磷酸化蛋白组学数据显示CC可能被MAPK信号系统成员MPK3/MPK6磷酸化，暗示MPK3/MPK6可能通过磷酸化向CC传递信号。在此基础上，本项目拟详细解析MPK3/MPK6磷酸化CC的调控机制，以及MPK3/MPK6-CC上游的信号感应器，期望构建一条细胞壁从感知到应答盐胁迫的信号调控途径，为阐明细胞壁在环境胁迫应答中的作用机制提供新的证据。

Environmental stresses threaten agricultural production. Understanding stress signaling and responses will increase our ability to improve stress resistance in crops. Cell wall plays critical roles in response to environmental stresses. Cellulose synthase complex, CSC, and its binding protein CC, COMPANION OF CELLULOSE SYNTHASE, sustain cellulose synthesis in cell wall during salt stress. The working model of CC-CSC has been elucidated clearly. However, how CC-CSC sense salt stress and signals are transduced remain unknown. In this project, we will study the signal transduce and regulatory mechanism of CC-CSC. We found several phosphorylated peptides of CC1 in a report identifying targets of MPK3/MPK6, two important members of Arabidopsis MAPK cascades, and also in our previous studies. These data imply the possibility that MPK3/MPK6 regulates CC-CSC through phosphorylating CC. So we will explore the regulatory mechanism of MPK3/MPK6 phosphorylating CC and identify the cell wall sensor(s) acting upstream of MPK3/MPK6-CC-CSC. The results will establish a cell wall signaling pathway in sensing and response to salt stress and provide evidence for understanding cell wall signaling in plants' environment stress responses.