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    Inducible XIST-dependent X-chromosome inactivation in human somatic cells is reversible

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    Authors
    Chow, Jennifer C.
    Hall, Lisa L.
    Baldry, Sarah E.L.
    Thorogood, Nancy P.
    Lawrence, Jeanne B.
    Brown, Carolyn J.
    UMass Chan Affiliations
    Department of Cell Biology
    Document Type
    Journal Article
    Publication Date
    2007-06-01
    Keywords
    Chromatin Immunoprecipitation
    Chromosomes, Human, X
    DNA Methylation
    DNA, Complementary
    *Dosage Compensation, Genetic
    Doxycycline
    Fibrosarcoma
    Gene Silencing
    Heterochromatin
    Histones
    Humans
    Immunohistochemistry
    In Situ Hybridization, Fluorescence
    Models, Genetic
    *RNA, Untranslated
    Sequence Analysis, DNA
    *X Chromosome Inactivation
    Cell Biology
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    Link to Full Text
    http://dx.doi.org/10.1073/pnas.0610946104
    Abstract
    During embryogenesis, the XIST RNA is expressed from and localizes to one X chromosome in females and induces chromosome-wide silencing. Although many changes to inactive X heterochromatin are known, the functional relationships between different modifications are not well understood, and studies of the initiation of X-inactivation have been largely confined to mouse. We now present a model system for human XIST RNA function in which induction of an XIST cDNA in somatic cells results in localized XIST RNA and transcriptional silencing. Chromatin immunoprecipitation and immunohistochemistry shows that this silencing need only be accompanied by a subset of heterochromatic marks and that these can differ between integration sites. Surprisingly, silencing is XIST-dependent, remaining reversible over extended periods. Deletion analysis demonstrates that the first exon of human XIST is sufficient for both transcript localization and the induction of silencing and that, unlike the situation in mice, the conserved repeat region is essential for both functions. In addition to providing mechanistic insights into chromosome regulation and formation of facultative heterochromatin, this work provides a tractable model system for the study of chromosome silencing and suggests key differences from mouse embryonic X-inactivation.
    Source
    Proc Natl Acad Sci U S A. 2007 Jun 12;104(24):10104-9. Epub 2007 May 30. Link to article on publisher's site
    DOI
    10.1073/pnas.0610946104
    Permanent Link to this Item
    http://hdl.handle.net/20.500.14038/36043
    PubMed ID
    17537922
    Related Resources
    Link to Article in PubMed
    ae974a485f413a2113503eed53cd6c53
    10.1073/pnas.0610946104
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