拟南芥蓝光受体CRY1通过高蓝光诱导的蛋白降解负反馈调控其信号转导的分子机理研究

Light is a critical environmental cue that profoundly regulates plant growth and development, which achieves its regulatory functions through light activated photoreceptors-mediated signal transduction pathways. Upon prolonged high intensity light illumination, plants undergo active light signaling, and for better developmental status, this process must be repressed by a negative regulatory mechanism. High light-induced degradation of photoreceptors can serve as such a mechanism. It is known that the red/far-red light photoreceptors phyB/phyA and the blue light photoreceptor CRY2 are degraded under high light. However, it is unknown whether CRY1, the major blue light photoreceptor that regulates photomorphogenesis under blue light, undergoes high blue light-induced degradation. Our preliminary results showed that CRY1 was degraded under high blue light, and that the blue light-triggered degradation of CRY1 was inhibited in the loss-of-function mutant of COP1, an E3 ubiquitin ligase. In addition, CRY1 interacts directly with BIC1, a repressor of CRY2 dimerization. We are planning to further study the molecular mechanism of blue-light-triggered degradation of CRY1 through molecular and biochemical approaches, hoping to reveal the negative feed-back regulatory mechanism of light signaling which allows plants to get adapted to high light condition and undergo normal growth and development.

光是调控植物生长发育的重要环境因子，它通过激活光受体启动信号转导来实现其调控作用。随着光照时间的延长或光照强度的增强，“高速运行”的光信号转导需要“刹车”来“减速”，否则不利于植物的生长发育。光受体的蛋白降解即可作为“刹车”来负反馈调控光信号转导。红光/远红光受体phyB/phyA、蓝光受体CRY2分别在强光下发生降解，但作为调控光形态建成的主要蓝光受体CRY1，其蛋白稳定性是否受强蓝光调控尚不清楚。申请人前期的工作表明，CRY1在高蓝光下发生蛋白降解。E3泛素连接酶COP1的突变导致高蓝光诱导的CRY1降解受到抑制，暗示CRY1降解与COP1有关。此外，CRY1与CRY2的二聚化抑制子BIC1发生互作。该项目拟通过分子和生化等手段进一步研究高蓝光依赖的CRY1降解调控的分子机理，以期揭示高蓝光信号通过负反馈调控光信号转导来优化植物的光形态建成，从而使植物适应高光环境的新机制。

光是调控植物生长发育的重要的环境因子。光激活的光受体通过介导信号转导调控植物的生长发育。随着光照时间的延长或光照强度的增强，“高速运行”的光信号转导需要通过“刹车”来“减速”，否则不利于植物的生长发育。光受体的蛋白降解即可作为“刹车”来抑制光信号转导。目前已知红光/远红光受体phyB/phyA、蓝光受体CRY2分别在强光下发生降解。但作为调控光形态建成的主要蓝光受体CRY1，其蛋白稳定性是否受强蓝光调控尚不清楚。我们的研究发现高强度蓝光能够特异地诱导CRY1蛋白发生泛素化并通过26S蛋白酶体降解。我们进一步发现光信号关键负调控元件，E3泛素连接酶COP1参与了CRY1在高强度蓝光下的泛素化进而促进其降解。此外，另一类E3泛素连接酶LRBs能够与CRY1在高强度蓝光下发生互作并参与CRY1在高强度蓝光下的泛素化和降解，最终在蓝光下促进拟南芥下胚轴的伸长。另外，蛋白互作实验表明CRY2寡聚化抑制蛋白BIC1也能够与CRY1发生蓝光依赖的互作。我们的研究进一步发现BIC1抑制高强度蓝光诱导的CRY1寡聚化，以及依赖于寡聚化的磷酸化和降解。该课题的研究揭示了CRY1在高强度蓝光下的蛋白稳态受到COP1，LRBs和BIC1在不同层面精细而严格的调控机制，该机制保证了植物能够根据环境中蓝光信号的强度合理的调控光形态建成的程度，最优化自身的生长发育状态。

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