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DNA Research Advance Access published online on January 11, 2006
DNA Research, doi:10.1093/dnares/dsi013
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© The Author 2006. Kazusa DNA Research Institute.
Received October 13, 2004
Revised March 12, 2005

Full Papers

XIST Repression in the Absence of DNMT1 and DNMT3B

Luciana R. Vasques 1, Raquel Stabellini 1, Fei Xue 2, X. Cindy Tian 2, Marina Soukoyan 1, and Lygia V. Pereira 1 *

1 Depto Biologia and Centro de Estudos do Genoma Humano, Instituto de Biociências, Universidade de São Paulo, São Paulo, SP 05508-900, Brazil
2 Center for Regenerative Biology/Department of Animal Science, University of Connecticut, Storrs, CT 06269, USA

* To whom correspondence should be addressed.
Lygia V. Pereira, E-mail: LPEREIRA{at}USP.BR


  Abstract

X chromosome inactivation (XCI) in human and mice involves XIST/Xist gene expression from the inactive X (Xi) and repression from the active X (Xa). Repression of the XIST/Xist gene on the Xa has been associated with methylation of its 5' region. In mice, Dnmt1 has been shown to be involved in the methylation and transcriptional repression of Xist on Xa. We examined maintenance of XIST gene repression on Xa in HCT116 cell lines knockout for either DNMT1 or DNMT3B and for DNMT1 and DNMT3B simultaneously. Methylation of the XIST promoter and XIST transcriptional repression is sustained in DNMT1-, DNMT3B- and DNMT1/DNMT3B knockout cells. Despite global DNA demethylation, the double knockout cells present only partial demethylation of the XIST promoter, which is not sufficient for gene reactivation. In contrast, global DNA demethylation with 5-aza-2'-deoxycytidine leads to XIST expression. Therefore, in these human cells maintenance of XIST methylation is controlled differently than global genomic methylation and in the absence of both DNMT1 and DNMT3B.

Keywords: X-chromosome inactivation; DNA-methyltransferase; XIST; epigenetic inheritance.
Communicated by Mitsuo Oshimura
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