Last, we investigated whether individual CpG sites within the studied regions (R1 to R6) showed specific correlation with either Mecp2 isoform (Figure 7B-C). Implicating the possible role of promoter R1 and R2 in mainly regulating Mecp2e1 (major isoform) at both D2 and D8, we observed a negative correlation between CpG methylation and Mecp2e1 expression at several CpG sites (r > -0.8, P <0.05) (Figure 7B, a, and 7C, a). At D2, unlike other REs, the average methylation over R3 showed an equally strong negative correlation with both Mecp2e1 (r = -0.94, P <0.05) and Mecp2e2 (r = -0.98, P <0.01) (Figure 7A, a). Therefore, we studied the two individual CpG sites located within R3 far apart from each other, which were differentially methylated (CpG1, approximately 10% and CpG2, approximately 30%) (Figure 6A, c). Interestingly, CpG1 showed a significant negative correlation with Mecp2e1 (r = -0.9, P <0.05), while CpG2 showed a significant negative correlation with Mecp2e2 (r = -0.9, P <0.01) (Figure 7B, c). Further confirming the potential role of these two CpG sites within R3 in Mecp2 isoform-specific expression,
