Integrated epigenomic analyses of neuronal MeCP2 reveal a role for long-range interaction with active genes

Dag H. Yasui, Sailaja Peddada, Mark C. Bieda, Roxanne O. Vallero, Amber Hogart, Raman P. Nagarajan, Karen N. Thatcher, Peggy J. Farnham, Janine M LaSalle

Research output: Contribution to journalArticle

286 Scopus citations


Mutations in MECP2 cause the autism-spectrum disorder Rett syndrome. MeCP2 is predicted to bind to methylated promoters and silence transcription. However, the first large-scale mapping of neuronal MeCP2-binding sites on 26.3 Mb of imprinted and non-imprinted loci revealed that 59% of MeCP2-binding sites are outside of genes and that only 6% are in CpG islands. Integrated genome-wide promoter analysis of MeCP2 binding, CpG methylation, and gene expression revealed that 63% of MeCP2-bound promoters are actively expressed and that only 6% are highly methylated. These results indicate that the primary function of MeCP2 is not the silencing of methylated promoters.

Original languageEnglish (US)
Pages (from-to)19416-19421
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Issue number49
StatePublished - Dec 4 2007



  • Chromatin
  • DNA methylation
  • Epigenetics
  • Genomics
  • Rett syndrome

ASJC Scopus subject areas

  • Genetics
  • General

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