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National Academy of Sciences, Proceedings of the National Academy of Sciences, 49(104), p. 19416-19421, 2007

DOI: 10.1073/pnas.0707442104

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

Journal article published in 2007 by Dag H. Yasui, Sailaja Peddada, Mark C. Bieda, Roxanne O. Vallero, Amber Hogart, Raman P. Nagarajan, Karen N. Thatcher, Peggy J. Farnham ORCID, Janine M. LaSalle
This paper is made freely available by the publisher.
This paper is made freely available by the publisher.

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Abstract

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 nonimprinted 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.