拟南芥RUP1与RUP2蛋白抑制UV-B光形态建成的机制研究

Light is one of the most important environmental cues for plant growth and development. Long-wavelength and low-fluence UV-B light is a newly defined light source that induces photomorphogenic development and beneficial agricultural features in plants. In recent years, extensive studies have been established on the promotive UV-B signaling machinery in the model plant Arabidopsis. However, it is poorly understood regarding the roles of two key repressors, RUP1 and RUP2. Our preliminary results have indicated that RUP1 and RUP2 might be recruited as substrate receptors into a multi-subunit E3 ligase complex for the proteasomal degradation of HY5, a central transcription factor in photomorphogenic UV-B signaling. This project will aim to investigate how RUP1 and RUP2 repress UV-B-induced photomorphogenesis and how UV-B light signal regulates the function of RUP1 and RUP2 to prevent an exaggerated response to light. Based on these studies, we will attempt to provide a biochemical insight into the repressive regulatory network of photomorphogenic UV-B signaling, and outline a fundamental mechanism by which the positive and negative regulators are intrinsically coordinated for an adequate and balanced photomorphogenic UV-B response.

光是调控植物生长发育最重要的环境因素之一。长波段、低强度的UV-B光诱导植物进行光形态建成，产生有利的农艺性状。RUP1与RUP2是UV-B光形态建成的负调控因子，然而它们如何抑制光信号转导的机制尚不清楚。本项目前期研究发现RUP1与RUP2具有E3泛素连接酶底物结合蛋白的结构特性，并能促进关键正调控转录因子HY5经由26S-蛋白酶体降解。因此，我们推测RUP1与RUP2可能通过参与E3泛素连接酶复合体来降解光形态建成促进因子从而负调控UV-B光信号转导。本项目拟通过研究RUP1与RUP2抑制作用方式以及二者如何受光信号调控，围绕RUP1与RUP2防止UV-B光信号过度放大这一核心问题，在生化层面上建立以RUP1与RUP2为基点的负调控信号网络，并通过研究二者与其它信号因子的功能关联，阐明UV-B光信号通路中正负调控因子协调作用，充分且平衡地进行光形态建成的分子机制。

光是自然界中影响动植物生命活动最重要的环境因子之一。光形态建成是植物响应环境光照的关键发育过程。长波段、低强度的UV-B光诱导植物进行光形态建成并产生有利的农艺性状。植物幼苗出土见光时不可避免地接受到越来越强的UV-B光照射。在此过程中，幼苗通过对UV-B光信号的感知与调节从而顺利地进行光形态建成。然而，植物中UV-B光信号转导的分子机制仍不明晰。本项目主要通过生物化学与遗传学的分析方法，解析了由两组泛素连接酶与一个转录因子组成的UV-B光信号转导途径。一方面，UV-B光诱导型蛋白RUP1/RUP2与泛素连接酶的骨架蛋白CUL4-DDB1组装成一个新型的泛素连接酶复合体，介导光信号转导通路的核心转录因子HY5蛋白的降解，从而抑制光形态建成。另一方面，COP1与RUP1/RUP2发生直接相互作用，介导RUP1/RUP2降解，使得RUP1/RUP2蛋白维持在适度水平。COP1与RUP1/RUP2的相互作用也削弱了COP1与HY5的相互作用。这些机制保护HY5不被降解而维持稳定，最终促进光形态建成。综上，本项目揭示了两组“泛素连接酶-底物”模块，即CUL4-DDB1-RUP1/RUP2-HY5与COP1-RUP1/RUP2，构成植物长时响应UV-B光信号的“抑制”与“去抑制”蛋白质机器，参与调控光形态建成的发育过程。本项目对植物中UV-B光信号转导的研究，有利于人们了解UV-B光照对植物生长发育的调控，推动UV-B光能源在农业生产与环境保护等人类基本社会活动中科学有效的应用。