SHB1与CLF互作调控植物光响应的研究

Light is one important environmental signal to plants. However, excess light damages photosynthetic apparatus and leads to photoinhibition. Plants acclimate a balanced state of photomorphogenesis to avoid photo-damage. We discovered a de-sensitization step involving up-regulation of PIF4 expression by SHB1 and CCA1 under red light. CCA1 brought circadian signals to the regulatory region of the PIF4 signaling hub. The integration of circadian signals with light signals was accomplished by CCA1 recruitment of SHB1. Recently, we verified an in vivo interaction of SHB1 with CLF and SWN. The expression of PIF4 is likely repressed in the dark by CLF and SWN PRC2 complex. SHB1 is thus recruited by CCA1 to antagonize CLF/SWN repression of PIF4 expression under red light. WRKY transcription factor MINI3 also binds a WRKY box nearby CCA1 binding site in PIF4 promoter and interacts directly with CCA1 but not SHB1. In this proposal, we will explore the repression of light-responsive genes in the dark by CLF and SWN, and this repression is inactivated by SHB1 under red light. We also investigate why MINI3 interacts with CCA1 and how MINI3 participates in the up-regulation of PIF4 expression. The proposed research will add new piece of information to our current understanding of light signaling and plant interaction with environment.

光照是植物生长不可缺的环境因子，但过多或过强的光照会对植物造成伤害，引起“光抑制”。植物要达到一种平衡的光形态建成状态以避免光伤害。本研究发现SHB1与CCA1互作并特异调控PIF4的表达以减弱光响应。CCA1将节律信号介入PIF4区域，而CCA1招募SHB1至此区域以整合节律信号和光信号。最近我们发现SHB1和CLF及SWN互作。CLF/SWN-PRC2复合体在黑暗中可能抑制PIF4表达，而红光下SHB1被CCA1招募至PIF4启动子拮抗CLF及SWN的抑制作用。MINI3也结合到一个临近CCA1结合位点的W-box, 直接与CCA1互作。本项目将解析黑暗条件下CLF/SWN抑制光响应基因表达及CLF/SWN和SHB1互作解除这种抑制的机制。同时，研究MINI3与CCA1互作在激活PIF4表达中的作用。本研究将对理解光信号传导及植物与环境互作提供重要信息。

光作为重要的信号因子调控植物生长发育。光信号通路中的PIF4能够通过整合光、温度和激素信号调控植物生长发育。PIF4的基因表达受到精准的调控。PIF4基因表达呈现昼夜规律和生物钟节律：在白天逐步升高；而在夜晚被抑制。在白天，CCA1、LHY通过招募转录激活因子SHB1激活PIF4表达。本研究发现两个WRKY转录因子WRKY2和WRKY10 (MINI3)能够直接结合PIF4启动子上的WRKY-box（W-box）。该W-box靠近CCA1的结合位点。在光下，WRKY2和WRKY10功能冗余地促进PIF4基因表达和下胚轴伸长。WRKY2和WRKY10能够与CCA1/LHY直接互作，并招募和促进CCA1/LHY结合到PIF4启动子上。光敏色素phyB通过与WRKY2和WRKY10直接互作，也促进CCA1/LHY结合PIF4启动子。WRKY2和WRKY10通过CCA1/LHY与SHB1间接互作。于是，在光下，存在phyB-WRKY2/10-CCA1/LHY-SHB1转录调控复合体精准调控PIF4基因表达。与此同时，SHB1能够直接上调WRKY2/WRKY10基因表达，进一步增强phyB-WRKY2/10-CCA1/LHY-SHB1转录调控复合体的含量。此项目支撑我们完成这一部分工作并取得重要成果，这有助于进一步阐释植物光信号调控植物生长的机理。