核孔蛋白Nup88调控植物光形态建成的分子机制

植物由暗形态建成到光形态建成的转换依赖于光敏色素通过核孔复合体从细胞质进入细胞核，激活光形态建成基因的表达，因此核孔蛋白对植物的光形态建成具有举足轻重的作用。但目前其调控光信号途径的机制尚不清楚。我们前期研究发现，核孔蛋白Nup88是光形态建成的正调控因子，且nup88突变体中光信号途径关键负调控因子光敏色素作用因子PIF1，3，4和5表达量均显著高于对照，因此推测Nup88通过PIFs调控植物光形态建成。基于此，本项目拟利用瞬时与稳定表达实验，明确Nup88对PIFs组织表达特异性、蛋白定位和含量的调控作用；利用酵母文库筛选Nup88的互作蛋白，并通过分子生物学的方法验证互作；利用过表达和敲除Nup88互作蛋白的遗传材料，明确其对下胚轴生长及PIFs的调控作用，以期揭示核孔蛋白Nup88调控植物光形态建成的分子机制，进而完善植物光形态建成的调控网络。

The transition from skotomorphogenesis to photomorphogenesis depends on translocation of photoreceptors and key regulators from the cytosol to the nucleus via Nuclear Pore Complexs (NPCs), therefore nucleoporins that make up NPCs are critical for photomorphogenesis. However, the mechanisms of nucleoporins in regulating photomorphogenesis remain elusive. Our previous studies have identified Nup88 as a positive regulator of photomorphogenesis. Expression of phytochrome interacting factors PIF1, 3, 4, and 5, key regulators of photomorphogenesis, are significantly increased in nup88 mutant as compared to wild type, which indicates a PIFs dependent regulatory role of Nup88 in photomorphogenesis. This project will continue based on the previous findings to examine whether the regulation of PIFs by Nup88 is exclusive to transcription or extends to tissue specificity, subcellular localization and protein abundance through transient and stable transformation. Then look for proteins that interact with Nup88 and validate the interactions with available molecular biology methods. Lastly, genetically clarify roles of Nup88 and its interaction protein in regulating hypocotyl growth by creating overexpressors and mutants. The project aims to elucidate molecular mechanisms of Nup88 in regulating photomorphogenesis, and extends the regulatory network of plant photomorphogenesis.