拟南芥磷脂酰肌醇特异性磷脂酶C1作为赤霉素次级应答组分参与开花时间调控的机制研究

磷脂酰肌醇特异性磷脂酶C1（PI-PLC1）催化磷脂酰肌醇-4,5-二磷酸水解为肌醇1,4,5-三磷酸（IP3）和二酰甘油（DAG）两个第二信使，传递细胞信号。根据缺失突变体plc1表现出的晚花表型，以及赤霉素诱导PLC1基因表达、部分挽救plc1晚花表型的前期结果。我们推测PLC1作为赤霉素信号的次级应答组分参与赤霉素途径对开花时间的调控。鉴于此，本研究通过表型观察，明确PLC1介导Ca2+调控植物开花；通过开花途径基因表达和转录组学分析，阐明PLC1影响植物开花的机制；通过染色质共沉淀和凝胶迁移实验，揭示DELLA蛋白对PLC1表达的直接调控作用；通过检测基因表达，DAG、IP3和Ca2+的含量，以及靶向代谢组学，明确PLC1在赤霉素途径中的地位及其对赤霉素合成代谢的反馈调节作用。该项目为完善植物开花调控机制中赤霉素途径的作用方式提供新的理论依据，为干预植物开花的应用提供新思路。

Phosphoinositide-specific phospholipase C1 (PI-PLC1) catalyzes the hydrolysis of phosphatidylinositol 4,5-bisphosphate into the two second messengers inositol 1,4,5-trisphosphate (IP3) and diacylglycerol (DAG), thus transmitting cell signals. According to the previous results of the late flowering of the deficient mutant plc1, gibberellin induced PLC1 gene expression and partially rescued late flowering of plc1. We speculate that PLC1, as a secondary response component of gibberellin signaling, is involved in the regulation of flowering by gibberellin pathway. This study intends to clarify the role of PLC1 in regulating flowering through Ca2+ by phenotypic observation; to elucidate the mechanism of PLC1 affecting flowering by gene expression and transcriptome analysis; to reveal the direct regulation of DELLA protein on PLC1 expression by chromatin immunoprecipitation and electrophoretic mobility shift assay; and to clarify the role of PLC1 in gibberellin pathway and its feedback regulation on gibberellin anabolism by detecting gene expression, the contents of DAG, IP3 and Ca2+, and the targeted metabonomics. This project provides a new theoretical basis for improving the function of gibberellin pathway in regulation mechanism of flowering and a new idea for the application of artificial intervention in flowering.