PGCs是配子的祖细胞，如有缺陷会使人和动物不育，它亦是家禽资源保存和转基因鸡制作的重要介质。但因其发育调控机制不明使其应用遇到了瓶颈。PGCs是从ESCs特化而来，两者DNA遗传信息相同但生物功能完全不同，说明表观遗传起了主要调控作用。本课题前期发现Lnc-PGC和H3K4me2参与鸡PGCs特化过程且共同靶向BMP基因和信号通路。故我们推测，可能H3K4me2甲基化修饰调控了Lnc-PGC的转录活性；也可能Lnc-PGC作为H3K4me2甲基化酶复合物的支架来调控启动子上的H3K4me2甲基化位点激活或抑制基因。故本课题拟将用功能缺失法继续追踪Lnc-PGC和H3K4me2甲基化作用及其与分化标记基因的关系；用分子生物学方法探索Lnc-PGC和H3K4me2甲基化的协同调控机制；揭示它们通过分化基因介导信号通路对ESCs分化为PGCs的双价调控作用，为家禽生产和人类生殖研究提供理论支撑

PGCs is the progenitor cell of all gametes, the lack of which will cause infertility in humans and animals, and it is also an important medium for the preservation of poultry resources and the production of transgenic chicken. However, since the mechanism of its development is unclear, its application has met an encountered bottleneck. PGCs is derived from ESCs, they have the same DNA genetic information but completely different biological functions, which indicated that epigenetic regulation plays an important role in PGCs development. In our previous study, we found that Lnc-PGC and H3K4me2 were involved in the differentiation of chicken ESCs into PGCs. Therefore, it was hypothesized that H3K4me2 methylation may activate or inhibit gene by regulating the transcriptional activity of Lnc-PGC，It aslo may be that Lnc-PGC acts as a scaffold for H3K4 methylase complex regulating the H3K4me2 methylation site on gene promoter to activate or inhibit gene expression. Therefore, the role of Lnc-PGC and H3K4 methylation and its relationship with target gene will be tracked by functional deletion method; Exploring the Synergistic Regulation of Lnc-PGC and H3K4me2 Methylation by Molecular Biology. The aim of this study was to reveal the mechanism of LncRNA and H3K4 modification to differentiate ESCs into PGCs, and to provide theoretical support for poultry egg production and human clinical reproductive research.