拟南芥SUMO E3连接酶SIZ1修饰WRKY33调控内质网胁迫应答的分子机制

植物内质网胁迫应答可缓解逆境引发的非正常折叠蛋白积累导致的细胞毒害，探究内质网胁迫应答分子机制对开展植物抗逆生物学研究具重要科学意义。目前有关内质网胁迫应答信号途径的研究多立足转录水平，翻译后修饰尤其是SUMO化修饰参与调控的研究资料甚少。本申请前期获得SUMO E3连接酶SIZ1的潜在靶蛋白WRKY33，初步证明WRKY33受内质网胁迫诱导并具应答特性，拟深入开展：1）分析SIZ1和WRKY33突变体和过表达株生理学表型，探究两者协同调控内质网胁迫应答特性；2）借助分子遗传、生物化学等技术，明确SIZ1和WRKY33互作机理及关键修饰位点，鉴定受其调控的内质网胁迫应答途径的关键基因；3）综合相关数据，探明WRKY33的SUMO化修饰对关键基因的调控作用，揭示SIZ1通过SUMO化修饰WRKY33调控内质网胁迫应答分子机制。预期研究有望丰富植物内质网胁迫应答途径和抗逆生物学理论内容与组成。

The endoplasmic reticulum (ER) stress response of plant can alleviate the cytotoxicity caused by the accumulation of unfolded or misfolded proteins in the adverse environment. Exploring the molecular mechanism of ER stress response is of great theoretical significance for the development of plant stress resistance biology. The current reported studies on ER stress response mainly focus on the transcriptional regulations, little is known about the protein post-tranlational modifications, especially SUMOylation (Small Ubiquitin-like Modifier, SUMO). We found that the potential SUMO-modified protein WRKY33 of SUMO E3 ligase SIZ1 could response to ER stress. The following in-depth research will be carried out: 1) Analyze the physiological phenotypes of mutants and overexpression plants, and explore the synergistically functions of SIZ1 and WRKY33 in ER stress response. 2) Using the molecular genetics and biochemical techniques, verify the protein interaction between SIZ1 and WRKY33, and the SUMOylation sites of WRKY33, and identify the key genes downstream of ER stress response signaling pathway regulated by WRKY33. 3) Clarify that the SUMOylation of WRKY33 could regulate the key genes of ER stress response pathways, and further reveal the molecular mechanism of SIZ1-mediated SUMOylation of WRKY33 in response to ER stress. Our research will provide theoretical evidence for plant ER stress response pathways and plant stress resistance biology.