微蛋白miP1c变构调控PIF1促进光介导种子萌发的分子机制研究

微蛋白是一类进化上保守、具有唯一蛋白结构域的小蛋白，作为重要的翻译后调节因子，快速抑制靶蛋白活性。PIF1（phytochrome interacting factor 1）是光介导种子萌发信号通路核心负调因子，见光后蛋白被降解。是否存在一类微蛋白变构调控PIF1蛋白活性，快速启动种子萌发，目前仍不清楚。我们前期研究发现微蛋白miP1a/b变构调控PIFs和EIN3蛋白自身四聚体活性，快速启动幼苗光形态建成。本研究在之前的基础上，发现一个新的微蛋白miP1c，见光后在种子中高表达，直接结合并在体外变构调控PIF1蛋白四聚化。本项目将重点研究微蛋白miP1c对靶标蛋白PIF1变构调控的分子机制，同时进一步完善miP1c-PIF1通路与已知HFR1-PIF1通路在种子萌发过程中的调控关系；旨在揭示微蛋白miP1c作为翻译后水平参与光介导种子萌发新的调控方式。

MicroProteins are evolutionarily conserved small single-domain proteins, acting as important post-translational regulators to rapidly inhibit their target proteins. PIF1 (phytochrome interacting factor 1), the key negative transcription regulator of light-induced seed germination, is induced to be degradation under light irradiation. It is still unclear whether there is a class of microProteins suppressing PIF1 protein activity to rapidly initiate seed germination. Our previous research find that two microProteins miP1a/b can disrupt the self-tetramer of PIFs and EIN3, and quickly initiate the photomorphogenic programs. Based on the previous study, a new microProtein miP1c is discovered. The experimental results show that miP1c is highly expressed in seeds under light irradiation, and can directly bind to PIF1 and allosterically regulate the tetramerization of PIF1 protein in vitro. This project will focus on the molecular mechanism analysis of microprotein miP1c allosterically regulating the target protein PIF1; then we will further explore the interaction between the candidate miP1c-PIF1 pathway with the known seed germination signal pathway HFR1-PIF1. It is proposed to reveal that microprotein miP1c acts as a new post-translational regulation of light-regulated seed germination.