Evidence that random and imprinted Xist expression is controlled by preemptive methylation

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 completel...

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Veröffentlicht in:Cell 1994-04, Vol.77 (1), p.41-51
Hauptverfasser: Norris, Dominic P., Patel, Dipika, Kay, Graham F., Penny, Graeme D., Brockdorff, Neil, Sheardown, Steven A., Rastan, Sohaila
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container_end_page 51
container_issue 1
container_start_page 41
container_title Cell
container_volume 77
creator Norris, Dominic P.
Patel, Dipika
Kay, Graham F.
Penny, Graeme D.
Brockdorff, Neil
Sheardown, Steven A.
Rastan, Sohaila
description 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.
doi_str_mv 10.1016/0092-8674(94)90233-X
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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. 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Psychology</topic><topic>Gene expression</topic><topic>Gene Expression Regulation</topic><topic>Humans</topic><topic>Imprinting (Psychology)</topic><topic>Male</topic><topic>Meiosis</topic><topic>Methylation</topic><topic>Mice</topic><topic>Mice, Inbred Strains</topic><topic>Molecular and cellular biology</topic><topic>Molecular genetics</topic><topic>RNA, Long Noncoding</topic><topic>RNA, Untranslated</topic><topic>Spermatozoa - metabolism</topic><topic>Transcription Factors - genetics</topic><topic>X Chromosome - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Norris, Dominic P.</creatorcontrib><creatorcontrib>Patel, Dipika</creatorcontrib><creatorcontrib>Kay, Graham F.</creatorcontrib><creatorcontrib>Penny, Graeme D.</creatorcontrib><creatorcontrib>Brockdorff, Neil</creatorcontrib><creatorcontrib>Sheardown, Steven A.</creatorcontrib><creatorcontrib>Rastan, Sohaila</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Nucleic Acids Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Cell</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Norris, Dominic P.</au><au>Patel, Dipika</au><au>Kay, Graham F.</au><au>Penny, Graeme D.</au><au>Brockdorff, Neil</au><au>Sheardown, Steven A.</au><au>Rastan, Sohaila</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Evidence that random and imprinted Xist expression is controlled by preemptive methylation</atitle><jtitle>Cell</jtitle><addtitle>Cell</addtitle><date>1994-04-08</date><risdate>1994</risdate><volume>77</volume><issue>1</issue><spage>41</spage><epage>51</epage><pages>41-51</pages><issn>0092-8674</issn><eissn>1097-4172</eissn><coden>CELLB5</coden><abstract>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. 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subjects Animals
Biological and medical sciences
Cell Differentiation
Dosage Compensation, Genetic
Female
Fundamental and applied biological sciences. Psychology
Gene expression
Gene Expression Regulation
Humans
Imprinting (Psychology)
Male
Meiosis
Methylation
Mice
Mice, Inbred Strains
Molecular and cellular biology
Molecular genetics
RNA, Long Noncoding
RNA, Untranslated
Spermatozoa - metabolism
Transcription Factors - genetics
X Chromosome - metabolism
title Evidence that random and imprinted Xist expression is controlled by preemptive methylation
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