MORC1 represses transposable elements in the mouse male germline

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. Clark () and Steven E. Jacobsen ()
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William A. Pastor: Cell and Developmental Biology, University of California Los Angeles
Hume Stroud: Cell and Developmental Biology, University of California Los Angeles
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
Steven E. Jacobsen: Cell and Developmental Biology, University of California Los Angeles

Nature Communications, 2014, vol. 5, issue 1, 1-14

Abstract: 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.

Date: 2014
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DOI: 10.1038/ncomms6795

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