Mecp2在斑马鱼胚胎神经发育中对NOTCH信号通路的调控

The Regulation of Mecp2 on Notch Signaling Pathway During Early Neural Development of Zebrafish Embryos

旨在探讨Mecp2在斑马鱼胚胎神经发育过程中的调控及机制。利用Notch转基因鱼,通过原位杂交技术和激光共聚焦显微技术发现Mecp2在胚胎发育过程前期广泛表达,随后逐渐表达在脑部。在敲低Mecp2的胚胎中,Notch信号的表达明显降低,注射Mecp2-RNA和胞内NICD-RNA均能够恢复这种表型,标记神经成熟的神经因子Ngn1、Pax2、Pax3、Eno2、Map和RNA结合蛋白HUC表达下调。在敲低Mecp2后其靶分子转录抑制因子Hey2表达下调,敲低Mecp2阻碍了神经细胞的正常分化成熟,结果表明Mecp2能够通过Notch-Hey2信号通路来调控斑马鱼神经细胞的分化。

This study aims to explore the regulation role and mechanism of Mecp2 during early neural development of zebrafish embryos. By the techniques of confocal laser scanning microscopy and in situ hybridization, and using Notch transgenic fish, it was found that Mecp2 widely expressed in the early embryonic development, then gradually expressed in the brain. In the embryos with Mcep2 knockdown, the expression of Notch signal decreased, and both the injection of Mcep2-RNA and intracellular INCD-RNA restored the phenotype. The expression of neural factors of Ngnl, Pax2, Pax3, Eno2, and Map labelling for neural maturation as well as HUC binding with RNA were downregulated. After Mecp2 knocked down, the expression of transcriptional repressor Hey2 downregulated because the knockdown hindered the differentiation and maturation of neural cells. Our study showed that Mecp2 regulated the differentiation of nerve ceils of zebrafish through Notch-Hey2 signaling pathways.