BR调节拟南芥转录因子BZR1核质穿梭的分子机理研究

油菜素内酯（BR）信号通路的核心转录因子BZR1具有核质穿梭特性：BR水平低时，BZR1在核中被磷酸化并被运出核；BR水平升高促进BZR1去磷酸化并在核中积累，但目前并不清楚BR水平升高时细胞核中积累的BZR1来自新合成的BZR1，还是将原有磷酸化出核的BZR1重新招募进核。此外BZR1进核是否依赖其自身的去磷酸化以及BR通过哪些蛋白调节BZR1进核也不清楚。本项目拟：1)利用光转换荧光蛋白Kaede来标记BZR1，实时观察BR调节BZR1进出核过程；2)检测不同突变形式BZR1蛋白的亚细胞定位和磷酸化状态对BR的响应；3)筛选调节BZR1核质穿梭的互作蛋白等研究手段来解析BR调节BZR1进出核的分子机制。本项目将填补BR信号转导途径的空白，拓展对胞外信号如何跨越核膜屏障机制的认识，为其他植物信号转导机制的研究提供重要的范例。

In the brassinosteroid (BR) signal transduction pathway, BRASSINAZOLE RESISTANT 1 (BZR1) family transcription factors play essential roles in mediating BR-regulated gene expression. The subcellular localization and transcriptional activity of BZR1 are tightly regulated by reversible protein phosphorylation; however, the underlying mechanism is unclear. Here we will study how BR signaling regulates the nucleocytoplasmic trafficking of BZR1 through 1）Real-time observe the BR regulated BZR1 nucleocytoplasmic trafficking process by photo convertible fluorescent protein, Kaede, tagged BZR1; 2）Observe the relationship between subcellular localization and phosphorylation state of different mutant BZR1; 3）Screen BZR1 interacting proteins which affect BZR1 nucleocytoplasmic trafficking. Our results will provide novel insight into BZR1 nucleocytoplasmic trafficking regulatory mechanisms, update our knowledge of BR signaling and may also provide clues about how signals transmit across the nuclear membranes, so inspire new studies in other fields.