小鼠部分肝切后的再生过程是在体研究静息细胞G0-G1转变与细胞周期调控的经典模型，但影响这一过程的转录调控机制仍未阐明。近年发展的染色质免疫共沉淀-质谱(ChIP-MS)分析技术可在基因组区域发现与修饰组蛋白结合的转录调控分子。课题组前期研究中对小鼠肝切后再生模型进行ChIP-MS、ChIP-seq和RNA-seq联合分析，筛选到受H3K27ac控制的甲基CpG结合蛋白2（MeCP2）可能在静息期肝细胞G0-G1的过渡中起重要作用，且发现MeCP2可能通过调节Jun-B表达影响肝细胞G0-G1过渡，提示MeCP2在细胞周期进程G0-G1过渡与肝再生过程中起重要作用。本项目拟通过肝细胞敲除MeCP2的小鼠与细胞模型，确定MeCP2在肝再生时静息期细胞G0-G1过渡中的作用，并通过转录调控分析技术，深入探讨其作用的细胞与分子机制，为细胞周期调控理论提供新观点，为促进肝脏再生提供新的潜在靶点。

The classical mouse model of liver regeneration (LR) after partial hepatectomy (PH) is a unique model allowing us to explore the organized mechanism which controls the G0-G1 transition and regulates cell cycle in vivo. However, the precise regulation mechanism of G0-G1 switch remains unclear. Chromatin immunoprecipitation-Mass spectrometry (ChIP-MS) is a recently developed novel technology to identify unprecedented proteins associated with genomic regions marked by modified histones. Combined the proteomics data from ChIP-MS, ChIP-seq and RNA-seq analyses of the mouse liver regeneration model, our previous study unveiled a novel factor, Methyl-CpG binding protein 2 (MeCP2), which is pivotal for the G0-G1 transition of quiescent hepatocytes, probably by regulating Jun-B expression. It implies that the MeCP2 plays an essential role in the G0-G1 transition and liver regeneration via cell cycle regulation. In this study, we aime to determine the role of MeCP2 in G0-G1 switch in liver regeneration through the liver specific MeCP2 knockout mouse model and explore the underlying mechanisms through transcriptional regulation analysis technology. These studies will extend our mechanistic understanding on cell cycle regulation and provide a new strategy for liver regeneration.