Differential Methylation of Xite and Ctcf Sites in Tsix Mirrors the Pattern of X-inactivation Choice in Mice.
From: Department of Molecular Biology, Howard Hughes Medical Institute, Massachusetts General Hospital, Simches 6.624, 185 Cambridge St., Boston, MA 02114, USA.
Molecular and cellular biology
- Publish Date: Mar 2006
- ISSN: 0270-7306
- Volume: 26
- Issue: 6
- Pages: 2109-17
- Medium: Print
- Language: English
- Citation (JAMA): Boumil Rebecca Maxfield, Ogawa Yuya, Sun Bryan K, et al. Differential Methylation of Xite and Ctcf Sites in Tsix Mirrors the Pattern of X-inactivation Choice in Mice.. Mol. Cell. Biol. Mar 2006;26:2109-17
Abstract
During mammalian dosage compensation, one of two X-chromosomes in female cells is inactivated. The choice of which X is silenced can be imprinted or stochastic. Although genetic loci influencing the choice decision have been identified, the primary marks for imprinting and random selection remain undefined. Here, we examined the role of DNA methylation, a mechanism known to regulate imprinting in autosomal loci, and sought to determine whether differential methylation on the two Xs might predict their fates. To identify differentially methylated domains (DMDs) at the X-inactivation center, we used bisulfite sequencing and methylation-sensitive restriction enzyme analyses. We found DMDs in Tsix and Xite, two genes previously shown to influence choice. Interestingly, the DMDs in Tsix lie within CTCF binding sites. Allelic methylation differences occur in gametes and are erased in embryonic stem cells carrying two active Xs. Because the pattern of DNA methylation mirrors events of X-inactivation, we propose that differential methylation of DMDs in Tsix and Xite constitute a primary mark for epigenetic regulation. The discovery of DMDs in CTCF sites draws further parallels between X-inactivation and autosomal imprinting.
Mesh Headings (Keywords): Animals, Binding Sites, Cell Differentiation, DNA Methylation, DNA-Binding Proteins, Female, Male, Mice, Mice, Inbred Strains, Mutation, Oocytes, RNA, Untranslated, Repressor Proteins, Spermatozoa, Stem Cells, X Chromosome Inactivation
Check for Full Text / PubMed Unique Identifier (PMID): 16507990
This abstract is part of PubMed, a service of the U.S. National Library of Medicine. PubMed includes more than 17 million citations from MEDLINE and other life science journals for biomedical articles. See Copyright and Disclaimers.
Linked medical terms appearing on this page are added by Healia to help readers find more information and are not part of the original PubMed document.
The data herein was last updated on July 8th, 2008 and may not reflect the most current and accurate data available from NLM.