The Mecp2 promoter CpG island studied by Franklin et al., [20] overlaps with the R1 and R2 of the Mecp2 promoter that we studied here. The significantly methylated CpGs reported in their study coincides with the R2 CpGs, where we observed changes at individual CpG sites as well as average methylation upon decitabine treatment. However, in our study we did not see any significant change in the R1 CpG sites (both D2 and D8), where Franklin et al., reported DNA methylation changes. Importantly, the results we obtained for one of the promoter regions studied (R2) are in agreement with this previous report, which showed a biological and functional importance of the methylation changes in regulating MeCP2 expression in response to stress in vivo. Therefore, it is likely that the detected changes we observed in the Mecp2 REs in our study also have biological importance. The hypermethylation of this R2 region in mouse brain was associated with MeCP2 downregulation [20], and hence it is possible that the hypomethylation/demethylation of the same R2 region causes Mecp2/MeCP2 upregulation.
