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    Maternal Rnf12/RLIM is required for imprinted X-chromosome inactivation in mice

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    Authors
    Shin, JongDae
    Bossenz, Michael
    Chung, Young
    Ma, Hong
    Byron, Meg
    Taniguchi-Ishigaki, Naoko
    Zhu, Xiaochun
    Baowei, Jiao
    Hall, Lisa L.
    Green, Michael R.
    Jones, Stephen N.
    Hermans-Borgmeyer, Irm
    Lawrence, Jeanne B.
    Bach, Ingolf
    Show allShow less
    UMass Chan Affiliations
    Program in Molecular Medicine
    Program in Gene Function and Expression
    Department of Cell Biology
    Document Type
    Journal Article
    Publication Date
    2010-10-22
    Keywords
    Animals
    Animals, Congenic
    Blastocyst
    Cell Line
    Chromosomes, Mammalian
    Embryo Loss
    Fathers
    Female
    Gene Silencing
    *Genomic Imprinting
    Male
    Mice
    Mice, Transgenic
    *Mothers
    RNA, Untranslated
    Repressor Proteins
    X Chromosome
    X Chromosome Inactivation
    Cell Biology
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    Link to Full Text
    http://dx.doi.org/10.1038/nature09457
    Abstract
    Two forms of X-chromosome inactivation (XCI) ensure the selective silencing of female sex chromosomes during mouse embryogenesis. Imprinted XCI begins with the detection of Xist RNA expression on the paternal X chromosome (Xp) at about the four-cell stage of embryonic development. In the embryonic tissues of the inner cell mass, a random form of XCI occurs in blastocysts that inactivates either Xp or the maternal X chromosome (Xm). Both forms of XCI require the non-coding Xist RNA that coats the inactive X chromosome from which it is expressed. Xist has crucial functions in the silencing of X-linked genes, including Rnf12 (refs 3, 4) encoding the ubiquitin ligase RLIM (RING finger LIM-domain-interacting protein). Here we show, by targeting a conditional knockout of Rnf12 to oocytes where RLIM accumulates to high levels, that the maternal transmission of the mutant X chromosome (Deltam) leads to lethality in female embryos as a result of defective imprinted XCI. We provide evidence that in Deltam female embryos the initial formation of Xist clouds and Xp silencing are inhibited. In contrast, embryonic stem cells lacking RLIM are able to form Xist clouds and silence at least some X-linked genes during random XCI. These results assign crucial functions to the maternal deposit of Rnf12/RLIM for the initiation of imprinted XCI.
    Source
    Nature. 2010 Oct 21;467(7318):977-81. Link to article on publisher's site
    DOI
    10.1038/nature09457
    Permanent Link to this Item
    http://hdl.handle.net/20.500.14038/36016
    Related Resources
    Link to Article in PubMed
    ae974a485f413a2113503eed53cd6c53
    10.1038/nature09457
    Scopus Count
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