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

Author

Listed:
  • JongDae Shin

    (Program in Gene Function and Expression, University of Massachusetts Medical School (UMMS))

  • Michael Bossenz

    (Centre for Molecular Neurobiology, University of Hamburg
    Present address: Institute for Biochemistry and Cell Biology, University of Magdeburg, 39120 Magdeburg, Germany.)

  • Young Chung

    (Stem Cell and Regenerative Medicine International, Inc.
    CHA University, School of Medicine)

  • Hong Ma

    (Program in Gene Function and Expression, University of Massachusetts Medical School (UMMS))

  • Meg Byron

    (UMMS)

  • Naoko Taniguchi-Ishigaki

    (Program in Gene Function and Expression, University of Massachusetts Medical School (UMMS))

  • Xiaochun Zhu

    (Program in Gene Function and Expression, University of Massachusetts Medical School (UMMS)
    Howard Hughes Medical Institute, UMMS)

  • Baowei Jiao

    (Program in Gene Function and Expression, University of Massachusetts Medical School (UMMS))

  • Lisa L. Hall

    (UMMS)

  • Michael R. Green

    (Program in Gene Function and Expression, University of Massachusetts Medical School (UMMS)
    Program in Molecular Medicine, UMMS
    Howard Hughes Medical Institute, UMMS)

  • Stephen N. Jones

    (UMMS)

  • Irm Hermans-Borgmeyer

    (Centre for Molecular Neurobiology, University of Hamburg)

  • Jeanne B. Lawrence

    (UMMS)

  • Ingolf Bach

    (Program in Gene Function and Expression, University of Massachusetts Medical School (UMMS)
    Program in Molecular Medicine, UMMS)

Abstract

Early X-chromosome silencing To ensure that female mammals do not have an excess of X-chromosome gene products, one of the two X chromosomes present in each cell is silenced. During embryogenesis, the imprinted form of this X-chromosome inactivation (XCI) process selectively silences the paternal X following the detection of Xist RNA expression on the paternal X chromosome (Xp) at about the four-cell stage of embryonic development. Later, an embryonic form of XCI occurs in the developing blastocyst of the embryo proper, inactivating either the paternal or maternal X chromosome at random. Using mouse genetics, Shin et al. show that maternal deposits of Rnf12/RLIM ubiquitin ligase are crucial in the initiation of the initial process, but not in the later random X inactivation.

Suggested Citation

  • JongDae Shin & Michael Bossenz & Young Chung & Hong Ma & Meg Byron & Naoko Taniguchi-Ishigaki & Xiaochun Zhu & Baowei Jiao & Lisa L. Hall & Michael R. Green & Stephen N. Jones & Irm Hermans-Borgmeyer , 2010. "Maternal Rnf12/RLIM is required for imprinted X-chromosome inactivation in mice," Nature, Nature, vol. 467(7318), pages 977-981, October.
    • Handle: RePEc:nat:nature:v:467:y:2010:i:7318:d:10.1038_nature09457
    DOI: 10.1038/nature09457
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    Cited by:

    1. Milan Kumar Samanta & Srimonta Gayen & Clair Harris & Emily Maclary & Yumie Murata-Nakamura & Rebecca M. Malcore & Robert S. Porter & Patricia M. Garay & Christina N. Vallianatos & Paul B. Samollow & , 2022. "Activation of Xist by an evolutionarily conserved function of KDM5C demethylase," Nature Communications, Nature, vol. 13(1), pages 1-16, December.
    2. Mariana I. Giassetti & Deqiang Miao & Nathan C. Law & Melissa J. Oatley & Julie Park & LeeLa D. Robinson & Lisette A. Maddison & Miranda L. Bernhardt & Jon M. Oatley, 2023. "ARRDC5 expression is conserved in mammalian testes and required for normal sperm morphogenesis," Nature Communications, Nature, vol. 14(1), pages 1-17, December.

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