光信号途径FHY3蛋白表达调控及信号转导分子机理研究

Light is one of the most important and basic environmental factors affecting plant growth and development. How the light signals are percepted by photoreceptors and transduced to the downstream components of light signaling pathway, and how these components transduced light signals to the nuclear targets and regulated its gene expression is one of the fundamental questions of light signaling studies. Recently, we showed how light signals affecting the entrainment of the circadian clock and flowering time regulation through FHY3, FAR1 and HY5, three positive regulators of the phytochrome A signaling pathway in Arabidopsis. We also characterized the transcriptional regulation network of FHY3 and identified ARC5 as one of the downstream targets of FHY3 which directly involved in chloroplast division. Conversely, How light signals transduced to FHY3 is still less well charcterized. Here, we will investigate the upstream signal transduction of FHY3 and address how the protein expression of FHY3 is generated and controlled by light and darkness, respectly. Whithin this project, we will demonstrate how the environmental light signals transduced from phyA to FHY3 and regulated its downstream gene expression. The molecular mechanism of FHY3 protein degradation and the molecular function of photomorgenesis suppressors in this process also will be characterized. Results from our studies could establish the molecular link between phyA and FHY3, and also will provide more evidences which could help us underlying the molecular mechanism of light regulated plant growth and development.

光是自然界中影响植物生长和发育最重要的环境因素之一。外界光信号如何通过光受体传递到下游信号蛋白，下游蛋白如何根据光信号变化调控植物生长发育，这些具体的信号转导分子机理是光信号研究的核心问题。近年来，申请人在光信号调控生物节律建成、开花时间调节, 及光信号途径关键转录因子FHY3的下游转录调控网络等方面进行了系统地研究并取得较好的研究进展。但外界光信号如何传递到FHY3，其分子调节机理仍不清楚。为此，在本项目中，我们将围绕 FHY3的上游信号途径展开，通过分别研究从黑暗到光下和从光下到黑暗FHY3蛋白表达调控和信号转导分子调节机理，着重解决外界环境光信号如何由光受体phyA传递到FHY3并调控下游基因表达和植物生长发育这一关键问题，阐明FHY3蛋白被26S蛋白酶体途径降解机理及光形态建成负调控因子在FHY3蛋白降解过程中的作用，进一步明确FHY3蛋白表达调控对植物生长发育的分子调节机理。

拟南芥光信号蛋白FHY3及其同源蛋白FAR1是由转座酶进化而来的一类特殊转录因子。已有研究结果证实，FHY3和FAR1通过调控远红光受体光敏色素A（phyA）的入核进而参与到远红光信号转导途径中，但FHY3蛋白本身的信号转导以及其下游转录调控机制仍不清晰。在本项目开展过程中，我们通过遗传学、生物化学和分子生物学等多种方法，主要针对FHY3蛋白与光受体phyA以及光形态建成负调控因子COP/DET类蛋白的相互作用展开研究，同时也针对FHY3和同源蛋白FAR1在植物肌醇代谢、氧化胁迫和淀粉代谢中的转录调控机制进行解析。主要研究结果如下：1)光信号蛋白FHY3的蛋白水平变化受到光信号的直接调控。FHY3蛋白在光下积累，在黑暗下快速降解，这与FHY3与光受体phyA，及光形态简称负调控因子COP/DET等蛋白的直接相互作用相关。2)FHY3和及其同源蛋白FAR1通过直接结合在下游基因肌醇磷酸合成酶MIPS1的启动子区域，进而调控肌醇合成和氧化胁迫适应。3)FHY3及其同源蛋白FAR1通过直接结合在下游基因淀粉去分支酶ISA2的启动子区域，进而调控光信号和糖信号介导的淀粉合成代谢。在项目开展过程中，圆满的完成了项目任务书中的各项研究任务，同时以本项目研究结果为基础，新申请并批准立项国家自然基金面上项目一项。在本项目资助下，已发表生物学一区杂志研究论文2篇，二区杂志论文1篇，SCI 影响因子合计18.8，待发表研究论文2篇。