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BIOLOGICAL SCIENCES / GENETICS
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^,, and Janine M. LaSalle^*,,¶

Departments of *Medical Microbiology and Immunology and Pharmacology, Rowe Program in Human Genetics, and Genome Center, School of Medicine, University of California, 1 Shields Avenue, Davis, CA 95616

Edited by Timothy H. Bestor, Columbia University, New York, NY, and accepted by the Editorial Board October 11, 2007 (received for review August 7, 2007)

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.

chromatin | DNA methylation | epigenetics | genomics | Rett syndrome

The authors declare no conflict of interest.

This article is a PNAS Direct Submission. T.H.B. is a guest editor invited by the Editorial Board.

Data deposition: The data reported in this paper have been deposited in the Gene Expression Omnibus (GEO) database, www.ncbi.nlm.nih.gov/geo (accession no. GSE9568).

This article contains supporting information online at www.pnas.org/cgi/content/full/0707442104/DC1.

^¶To whom correspondence should be addressed. E-mail: jmlasalle{at}ucdavis.edu

© 2007 by The National Academy of Sciences of the USA

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