TMK介导的生长素信号途径调控植物高温胁迫响应的分子机制

全球变暖成为农业生产的巨大威胁，环境温度升高导致农作物正遭受越来越棘手的高温胁迫，研究植物高温响应调节机制迫在眉睫。生长素不仅对植物生长发育的调控至关重要，而且在植物响应复杂环境过程中发挥关键作用，然而其中机制知之甚少。我们的研究发现，生长素参与植物高温响应，且生长素信号途径关键因子TMK1对于植物高温响应至关重要，其突变体呈现对高温不耐受的响应缺陷。通过蛋白质组学和生化分析显示TMK1和热激转录共激活因子MBF1c特异性互作，且TMK1直接磷酸化MBF1c第十位苏氨酸；MBF1c的磷酸化提高了其结合DREB2A启动子区的亲和力；更重要的是，TMK1磷酸化MBF1c是其行使高温胁迫响应所必需。本课题拟在此基础上，进一步解析TMK1-MBF1c通路是否介导生长素信号响应高温胁迫并深入剖析其分子机制，将为改善植物耐高温提供新的研究策略。

The high temperature damages the production of crops, which becomes more serious in recent years. It is urgent to explore the novel mechanisms of plant responses to high temperature. Auxin, one of the pivotal hormones in plant, plays important roles in regulation of plant growth and stress responses. However, it is still unclear how auxin signaling elaborately regulate environment stress responses. Our recent study found that TMK1, a key component in auxin signaling, participates in high temperature stress responses. tmk1 mutant displays hypersensitive to high temperature and lower survival rates comparing with wild type and other tmks mutants. We also showed that TMK1 directly interacts with MBF1c, which is a key transcriptional coactivator in plant high temperature signaling pathway. Furthermore, TMK1 can directly phosphorylate MBF1c at Thr10, and the phosphor-mimic of MBF1c enhance its DNA binding affinity to the promoter of DREB2A. More importantly, the phosphorylation of MBF1c by TMK1 at Thr10 is required for its function in heat temperature stress responses. In this proposal, we will further explore the molecular mechanisms of TMK1-MBF1c in responses to high temperature and auxin-TMK1 signaling transduction in regulation of MBF1c function in heat signaling. This will provide potential molecular strategy for improving plant thermotolerance.