qGL3-OsGSK3-OsFCA通路调控水稻籽粒大小和开花时间的分子机制研究

油菜素甾醇（BR）对于水稻籽粒大小等多种农艺性状具有重要的调控作用，但其调控机制和关键基因仍有待于深入研究和挖掘。本实验室前期克隆了水稻粒长QTL位点qGL3，该位点编码一个蛋白磷酸酶，通过去磷酸化蛋白激酶OsGSK3负调控水稻BR信号和粒长。通过磷酸化蛋白质组学技术，我们发现拟南芥开花调控蛋白FCA的水稻同源蛋白OsFCA的磷酸化水平在qGL3缺失突变体和NIL-qgl3近等基因系中显著上调。OsFCA不能与qGL3互作，但可以与OsGSK3互作，并被OsGSK3磷酸化。osfca突变体的植株变矮、籽粒变小，对BR处理钝感；敲除OsFCA能够显著抑制OsGSK3缺失突变体的BR增强表型，表明OsFCA可能作用于OsGSK3的下游并正调控BR信号。本项目将在已有研究基础上揭示一个新的qGL3-OsGSK3-OsFCA信号通路，并解析BR如何通过该通路调控水稻籽粒大小和开花时间。

Brassinosteroids (BRs) play critical roles in the regulations of multiple rice agronomic traits including plant height, tiller number, grain size, etc. However, the mechanism and gene network of BR signaling are still largely unknown. We previously cloned qGL3, a major QTL for grain length in rice. qGL3 encodes a protein phosphatase which dephosphorylates protein kinase OsGSK3 to negatively regulate BR signaling and grain length. We further found that the phosphorylation level of OsFCA, an orthologue of Arabidopsis FLOWERING CONTROL LOCUS A(FCA) in rice, was significantly increased in qGL3-knocking out mutant and NIL-qgl3. OsFCA cannot physically interact with qGL3, but it interacts with and is phosphorylated by OsGSK3. Compared with wild-type, the osfca mutant reduced plant height, grain size, the tiller number and the sensitivity to exogenous treatment of BL. Knocking-out OsFCA significantly suppressed the BR-enhanced phenotypes observed in OsGSK3 knocking-out mutant, suggesting that OsFCA functions downstream of OsGSK3 to positively regulate BR signaling. This project aims to clarify a novel qGL3-OsGSK3-OsFCA pathway and decipher how BR signaling modulates grain size and flowering time through this pathway.