Variable escape from X-chromosome inactivation: Identifying factors that tip the scales towards expression

In humans over 15% of X‐linked genes have been shown to ‘escape’ from X‐chromosome inactivation (XCI): they continue to be expressed to some extent from the inactive X chromosome. Mono‐allelic expression is anticipated within a cell for genes subject to XCI, but random XCI usually results in express...

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Published inBioEssays Vol. 36; no. 8; pp. 746 - 756
Main Authors Peeters, Samantha B., Cotton, Allison M., Brown, Carolyn J.
Format Journal Article
LanguageEnglish
Published United States Blackwell Publishing Ltd 01.08.2014
Wiley Subscription Services, Inc
Subjects
allelic imbalance
Animals
boundary elements
Chromosomes
Chromosomes, Human, X - genetics
Chromosomes, Human, X - ultrastructure
DNA Methylation
dosage compensation
epigenetic marks
Evolution, Molecular
Gene Expression
Genes
Genes, X-Linked
Humans
Inactivation
Prospects & Overviews
RNA-seq
Topology
waystations
X Chromosome Inactivation
XIST
waystations
RNA-seq
boundary elements
XIST
allelic imbalance
dosage compensation
epigenetic marks
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Abstract In humans over 15% of X‐linked genes have been shown to ‘escape’ from X‐chromosome inactivation (XCI): they continue to be expressed to some extent from the inactive X chromosome. Mono‐allelic expression is anticipated within a cell for genes subject to XCI, but random XCI usually results in expression of both alleles in a cell population. Using a study of allelic expression from cultured lymphoblasts and fibroblasts, many of which showed substantial skewing of XCI, we recently reported that the expression of genes lies on a contiunuum between those that are subject to inactivation, and those that escape. We now review allelic expression studies from mouse, and discuss the variability in escape seen in both humans and mice in genic expression levels, between X chromosomes and between tissues. We also discuss current knowledge of the heterochromatic features, DNA elements and three‐dimensional topology of the inactive X that contribute to the balance of expression from the otherwise inactive X chromosome. Incomplete transcriptional silencing of X‐chromosome inactivation (XCI) results in some genes being variably expressed from the inactive X, with differences seen between females and between tissues. The variable expression likely reflects the impact of factors contributing to XCI, including DNA sequences, chromatin features, and 3D architecture of the chromosome.
AbstractList In humans over 15% of X‐linked genes have been shown to ‘escape’ from X‐chromosome inactivation (XCI): they continue to be expressed to some extent from the inactive X chromosome. Mono‐allelic expression is anticipated within a cell for genes subject to XCI, but random XCI usually results in expression of both alleles in a cell population. Using a study of allelic expression from cultured lymphoblasts and fibroblasts, many of which showed substantial skewing of XCI, we recently reported that the expression of genes lies on a contiunuum between those that are subject to inactivation, and those that escape. We now review allelic expression studies from mouse, and discuss the variability in escape seen in both humans and mice in genic expression levels, between X chromosomes and between tissues. We also discuss current knowledge of the heterochromatic features, DNA elements and three‐dimensional topology of the inactive X that contribute to the balance of expression from the otherwise inactive X chromosome. Incomplete transcriptional silencing of X‐chromosome inactivation (XCI) results in some genes being variably expressed from the inactive X, with differences seen between females and between tissues. The variable expression likely reflects the impact of factors contributing to XCI, including DNA sequences, chromatin features, and 3D architecture of the chromosome.
In humans over 15% of X-linked genes have been shown to 'escape' from X-chromosome inactivation (XCI): they continue to be expressed to some extent from the inactive X chromosome. Mono-allelic expression is anticipated within a cell for genes subject to XCI, but random XCI usually results in expression of both alleles in a cell population. Using a study of allelic expression from cultured lymphoblasts and fibroblasts, many of which showed substantial skewing of XCI, we recently reported that the expression of genes lies on a contiunuum between those that are subject to inactivation, and those that escape. We now review allelic expression studies from mouse, and discuss the variability in escape seen in both humans and mice in genic expression levels, between X chromosomes and between tissues. We also discuss current knowledge of the heterochromatic features, DNA elements and three-dimensional topology of the inactive X that contribute to the balance of expression from the otherwise inactive X chromosome.In humans over 15% of X-linked genes have been shown to 'escape' from X-chromosome inactivation (XCI): they continue to be expressed to some extent from the inactive X chromosome. Mono-allelic expression is anticipated within a cell for genes subject to XCI, but random XCI usually results in expression of both alleles in a cell population. Using a study of allelic expression from cultured lymphoblasts and fibroblasts, many of which showed substantial skewing of XCI, we recently reported that the expression of genes lies on a contiunuum between those that are subject to inactivation, and those that escape. We now review allelic expression studies from mouse, and discuss the variability in escape seen in both humans and mice in genic expression levels, between X chromosomes and between tissues. We also discuss current knowledge of the heterochromatic features, DNA elements and three-dimensional topology of the inactive X that contribute to the balance of expression from the otherwise inactive X chromosome.
In humans over 15% of X-linked genes have been shown to ‘escape’ from X-chromosome inactivation (XCI): they continue to be expressed to some extent from the inactive X chromosome. Mono-allelic expression is anticipated within a cell for genes subject to XCI, but random XCI usually results in expression of both alleles in a cell population. Using a study of allelic expression from cultured lymphoblasts and fibroblasts, many of which showed substantial skewing of XCI, we recently reported that the expression of genes lies on a contiunuum between those that are subject to inactivation, and those that escape. We now review allelic expression studies from mouse, and discuss the variability in escape seen in both humans and mice in genic expression levels, between X chromosomes and between tissues. We also discuss current knowledge of the heterochromatic features, DNA elements and three-dimensional topology of the inactive X that contribute to the balance of expression from the otherwise inactive X chromosome.
In humans over 15% of X-linked genes have been shown to 'escape' from X-chromosome inactivation (XCI): they continue to be expressed to some extent from the inactive X chromosome. Mono-allelic expression is anticipated within a cell for genes subject to XCI, but random XCI usually results in expression of both alleles in a cell population. Using a study of allelic expression from cultured lymphoblasts and fibroblasts, many of which showed substantial skewing of XCI, we recently reported that the expression of genes lies on a contiunuum between those that are subject to inactivation, and those that escape. We now review allelic expression studies from mouse, and discuss the variability in escape seen in both humans and mice in genic expression levels, between X chromosomes and between tissues. We also discuss current knowledge of the heterochromatic features, DNA elements and three-dimensional topology of the inactive X that contribute to the balance of expression from the otherwise inactive X chromosome. Incomplete transcriptional silencing of X-chromosome inactivation (XCI) results in some genes being variably expressed from the inactive X, with differences seen between females and between tissues. The variable expression likely reflects the impact of factors contributing to XCI, including DNA sequences, chromatin features, and 3D architecture of the chromosome.
In humans over 15% of X-linked genes have been shown to 'escape' from X-chromosome inactivation (XCI): they continue to be expressed to some extent from the inactive X chromosome. Mono-allelic expression is anticipated within a cell for genes subject to XCI, but random XCI usually results in expression of both alleles in a cell population. Using a study of allelic expression from cultured lymphoblasts and fibroblasts, many of which showed substantial skewing of XCI, we recently reported that the expression of genes lies on a contiunuum between those that are subject to inactivation, and those that escape. We now review allelic expression studies from mouse, and discuss the variability in escape seen in both humans and mice in genic expression levels, between X chromosomes and between tissues. We also discuss current knowledge of the heterochromatic features, DNA elements and three-dimensional topology of the inactive X that contribute to the balance of expression from the otherwise inactive X chromosome. [PUBLICATION ABSTRACT]
Author Peeters, Samantha B.
Brown, Carolyn J.
Cotton, Allison M.
Author_xml – sequence: 1
  givenname: Samantha B.
  surname: Peeters
  fullname: Peeters, Samantha B.
  organization: Department of Medical Genetics, Molecular Epigenetics Group, Life Sciences Institute, University of British Columbia, BC, Vancouver, Canada
– sequence: 2
  givenname: Allison M.
  surname: Cotton
  fullname: Cotton, Allison M.
  organization: Department of Medical Genetics, Molecular Epigenetics Group, Life Sciences Institute, University of British Columbia, BC, Vancouver, Canada
– sequence: 3
  givenname: Carolyn J.
  surname: Brown
  fullname: Brown, Carolyn J.
  email: Carolyn J. Brown, cbrown@mail.ubc.ca
  organization: Department of Medical Genetics, Molecular Epigenetics Group, Life Sciences Institute, University of British Columbia, BC, Vancouver, Canada
BackLink https://www.ncbi.nlm.nih.gov/pubmed/24913292$$D View this record in MEDLINE/PubMed
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Issue 8
Keywords waystations
RNA-seq
boundary elements
XIST
allelic imbalance
dosage compensation
epigenetic marks
Language English
License Attribution-NonCommercial-NoDerivs
2014 The Authors. Bioessays published by WILEY Periodicals, Inc.
This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
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2010; 11
2012; 121
2012; 485
2012; 487
2006; 38
2002; 12
2004; 7
2002; 11
2002; 99
1999; 286
2014; 24
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1991; 349
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2012; 22
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2013; 500
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1999; 21
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1994; 368
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2013; 30
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2003; 300
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SecondaryResourceType review_article
Snippet In humans over 15% of X‐linked genes have been shown to ‘escape’ from X‐chromosome inactivation (XCI): they continue to be expressed to some extent from the...
In humans over 15% of X-linked genes have been shown to 'escape' from X-chromosome inactivation (XCI): they continue to be expressed to some extent from the...
In humans over 15% of X-linked genes have been shown to ‘escape’ from X-chromosome inactivation (XCI): they continue to be expressed to some extent from the...
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pubmed
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wiley
istex
SourceType Open Access Repository
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StartPage 746
SubjectTerms allelic imbalance
Animals
boundary elements
Chromosomes
Chromosomes, Human, X - genetics
Chromosomes, Human, X - ultrastructure
DNA Methylation
dosage compensation
epigenetic marks
Evolution, Molecular
Gene Expression
Genes
Genes, X-Linked
Humans
Inactivation
Prospects & Overviews
RNA-seq
Topology
waystations
X Chromosome Inactivation
XIST
Title Variable escape from X-chromosome inactivation: Identifying factors that tip the scales towards expression
URI https://api.istex.fr/ark:/67375/WNG-9F89141J-F/fulltext.pdf
https://onlinelibrary.wiley.com/doi/abs/10.1002%2Fbies.201400032
https://www.ncbi.nlm.nih.gov/pubmed/24913292
https://www.proquest.com/docview/1553146842
https://www.proquest.com/docview/1547542615
https://www.proquest.com/docview/1566832319
https://pubmed.ncbi.nlm.nih.gov/PMC4143967
Volume 36
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