MIP1介导的茉莉酸信号通路MED25蛋白稳定性和转录活性调控的功能研究

茉莉酸是一种重要的植物激素，其信号转导的实质是以MYC2为代表的转录因子所参与的转录重编程过程。在激活MYC2的过程中，中介体亚基MED25作为桥梁蛋白连接MYC2和RNA聚合酶Pol II，对MYC2下游靶基因表达至关重要。项目前期的研究表明：26S蛋白酶体途径介导的MED25降解与其激活MYC2转录活性密切相关。然而，MED25降解偶联激活MYC2转录活性的分子机制仍不清楚。本申请将以MED25在JA信号通路中发生转录激活功能需要其蛋白发生降解为切入点展开研究。一方面，围绕可与MED25 vWFA结构域互作的MIP1及MBR1/2 (降解MED25的E3泛素连接酶)如何拮抗调节MED25的稳定性及如何参与JA信号通路的调节进行研究；另一方面，建立MED25蛋白降解和激活MYC2转录活性之间的内在联系，为解析MED25如何激活MYC2转录活性的分子机制奠定基础，丰富对茉莉酸信号通路的认识。

Jasmonaic Acid (JA) is an important plant hormone，the essence of its signal transduction is MYC2-directed transcription reprogramming, and MED25 plays a key role during this process by connecting MYC2 and RNA polymerase II. Our previous studies illustrated that 26S proteasome-mediated MED25 degradation is coupled with its transcription co-activation function. However，what is the molecular mechanism of MED25 turnover activates transcription activity of MYC2 in JA signaling pathway remain unknown. In this application, by using the MED25 turnover is coupled to its function as a entry point, on the one hand, we propose to study MIP1 and MBR1/2 (E3 ligases for MED25), all interact with MED25 through vWFA domain, are involved in the regulation the stability of MED25 and JA signaling pathway, on the other hand, we will to establish the inner connection between protein stability and transcription co-activation activity. This application will dissect the molecular mechanism of how MED25 activates MYC2 target genes expression, and complete the understanding of JA signaling pathway.