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The mouse Xist gene is expressed exclusively from the inactive X chromosome and may control the initiation of X inactivation. We show that in somatic tissues the 5' end of the silent Xist allele on the active X chromosome is fully methylated, while the expressed allele on the inactive X is completely unmethylated. In tissues that undergo imprinted paternal Xist expression and imprinted X inactivation, the paternal Xist allele is unmethylated, and the silent maternal allele is fully methylated. In the male germline, a developmentally regulated demethylation of Xist occurs at the onset of meiosis and is retained in mature spermatozoa. This may be the cause of imprinted expression of the paternal Xist allele. A role for methylation in the control of Xist expression is further supported by the finding that in differentiating embryonic stem cells during the initiation of X inactivation, differential methylation of Xist alleles precedes the onset of Xist expression.

Original publication

DOI

10.1016/0092-8674(94)90233-x

Type

Journal article

Journal

Cell

Publication Date

08/04/1994

Volume

77

Pages

41 - 51

Keywords

Animals, Cell Differentiation, Dosage Compensation, Genetic, Female, Gene Expression Regulation, Humans, Imprinting (Psychology), Male, Meiosis, Methylation, Mice, Mice, Inbred Strains, RNA, Long Noncoding, RNA, Untranslated, Spermatozoa, Transcription Factors, X Chromosome