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MORC1 represses transposable elements in the mouse male germline

Author

Listed:
  • William A. Pastor

    (Cell and Developmental Biology, University of California Los Angeles)

  • Hume Stroud

    (Cell and Developmental Biology, University of California Los Angeles
    Present address: Department of Neurobiology, Harvard Medical School, 220 Longwood Avenue, Boston, Massachusetts 02115 USA)

  • Kevin Nee

    (Cell and Developmental Biology, University of California Los Angeles)

  • Wanlu Liu

    (Cell and Developmental Biology, University of California Los Angeles)

  • Dubravka Pezic

    (California Institute of Technology)

  • Sergei Manakov

    (California Institute of Technology)

  • Serena A. Lee

    (Cell and Developmental Biology, University of California Los Angeles)

  • Guillaume Moissiard

    (Cell and Developmental Biology, University of California Los Angeles)

  • Natasha Zamudio

    (Unité de génétique et biologie du développement, Instititute Curie)

  • Déborah Bourc’his

    (Unité de génétique et biologie du développement, Instititute Curie)

  • Alexei A. Aravin

    (California Institute of Technology)

  • Amander T. Clark

    (Cell and Developmental Biology, University of California Los Angeles
    Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research, University of California Los Angeles)

  • Steven E. Jacobsen

    (Cell and Developmental Biology, University of California Los Angeles
    Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research, University of California Los Angeles
    Howard Hughes Medical Institute, University of California Los Angeles)

Abstract

The Microrchidia (Morc) family of GHKL ATPases are present in a wide variety of prokaryotic and eukaryotic organisms but are of largely unknown function. Genetic screens in Arabidopsis thaliana have identified Morc genes as important repressors of transposons and other DNA-methylated and silent genes. MORC1-deficient mice were previously found to display male-specific germ cell loss and infertility. Here we show that MORC1 is responsible for transposon repression in the male germline in a pattern that is similar to that observed for germ cells deficient for the DNA methyltransferase homologue DNMT3L. Morc1 mutants show highly localized defects in the establishment of DNA methylation at specific classes of transposons, and this is associated with failed transposon silencing at these sites. Our results identify MORC1 as an important new regulator of the epigenetic landscape of male germ cells during the period of global de novo methylation.

Suggested Citation

  • William A. Pastor & Hume Stroud & Kevin Nee & Wanlu Liu & Dubravka Pezic & Sergei Manakov & Serena A. Lee & Guillaume Moissiard & Natasha Zamudio & Déborah Bourc’his & Alexei A. Aravin & Amander T. Cl, 2014. "MORC1 represses transposable elements in the mouse male germline," Nature Communications, Nature, vol. 5(1), pages 1-14, December.
    • Handle: RePEc:nat:natcom:v:5:y:2014:i:1:d:10.1038_ncomms6795
    DOI: 10.1038/ncomms6795
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    Cited by:

    1. Sophia Groh & Anna Viktoria Milton & Lisa Katherina Marinelli & Cara V. Sickinger & Angela Russo & Heike Bollig & Gustavo Pereira de Almeida & Andreas Schmidt & Ignasi Forné & Axel Imhof & Gunnar Scho, 2021. "Morc3 silences endogenous retroviruses by enabling Daxx-mediated histone H3.3 incorporation," Nature Communications, Nature, vol. 12(1), pages 1-18, December.

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