for MeCP2 deficiency-related neurodevelopmental disorders such as autism and Rett syndrome. Finally, the significant and dynamic (positive or negative) correlation between the expression of Mecp2 isoforms and DNA methylation implies the potential contribution of these REs in regulating Mecp2 isoforms at different stages of neural differentiation. Collectively, our study contributes to the understanding of expression and regulation of Mecp2 isoforms during neural development and provides important insights for future therapeutic applications of decitabine for MeCP2-related neurological disorders.
