Intragenic DNA methylation modulates alternative splicing by recruiting MeCP2 to promote exon recognition [ChIP-Seq]

ABSTRACT: Although the function of DNA methylation in gene promoter regions is well established in transcriptional repression, the function of the evolutionarily conserved widespread distribution of DNA methylation in gene body regions remains incompletely understood. Here, we show that DNA methylation is enriched in included alternatively spliced exons (ASEs) and inhibiting DNA methylation results in aberrant splicing of ASEs. The methyl-CpG binding protein MeCP2 is enriched in included ASEs, particularly those that are also highly DNA methylated, and inhibition of DNA methylation disrupts specific targeting of MeCP2 to exons. Interestingly, ablation of MeCP2 results in increased nucleosome acetylation and aberrant skipping events of ASEs. We further show that inhibition of histone deacetylases lea

ORGANISM(S): Homo sapiens

SUBMITTER: Iouri Chepelev 

PROVIDER: E-GEOD-47677 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress