The intron 1 regions analyzed in this study were designated as part of a silencer element, which has been previously proposed to regulate MECP2 alternative splicing and tissue-specific expression [12]. Our findings are in agreement with possible involvement of these regions in Mecp2 isoform-specific expression. Although the link between DNA methylation and Mecp2 expression is supported by our results in the NSC system, the contribution of other epigenetic modifications such as histone acetylation and histone methylation should not be excluded [73,74].
