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Nucleic Acids Research Advance Access published online on October 20, 2009
Nucleic Acids Research, doi:10.1093/nar/gkp860
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© The Author(s) 2009. Published by Oxford University Press.
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.5/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Gene Regulation, Chromatin and Epigenetics

Inactive X chromosome-specific histone H3 modifications and CpG hypomethylation flank a chromatin boundary between an X-inactivated and an escape gene

Yuji Goto1,2 and Hiroshi Kimura1,3,*

1Nuclear Function and Dynamics Unit, Horizontal Medical Research Organization, Graduate School of Medicine, Kyoto University, Sakyo-ku, Kyoto 606-8501, 2College of Life and Health Sciences, Chubu University, Kasugai, Aichi 487-8501 and 3Graduate School of Frontier Biosciences, Osaka University, 1-3 Yamadaoka, Suita, Osaka 565-0871, Japan

*To whom correspondence should be addressed. Tel: +81 6 6879 4623; Fax: +81 6 6879 4622; Email: hkimura{at}fbs.osaka-u.ac.jp

Received August 6, 2009. Revised September 24, 2009. Accepted September 26, 2009.

In mammals, the dosage compensation of sex chromosomes between males and females is achieved by transcriptional inactivation of one of the two X chromosomes in females. However, a number of genes escape X-inactivation in humans. It remains poorly understood how the transcriptional activity of these ‘escape genes’ is maintained despite the chromosome-wide heterochromatin formation. To address this question, we analyzed a putative chromatin boundary between the inactivated RBM10 and an escape gene, UBA1/UBE1. Chromatin immunoprecipitation revealed that trimethylated histone H3 lysine 9 and H4 lysine 20 were enriched in the last exon through the proximal downstream region of RBM10, but were remarkably diminished at ~2 kb upstream of the UBA1 transcription start site. Whereas RNA polymerase II was not loaded onto the intergenic region, CTCF (CCCTC binding factor) was enriched around the boundary, where some CpG sites were hypomethylated specifically on inactive X. These findings suggest that local DNA hypomethylation and CTCF binding are involved in the formation of a chromatin boundary, which protects the UBA1 escape gene against the chromosome-wide transcriptional silencing.


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