MORC1 represses transposable elements in the mouse male germline.

Nat Commun

1] Department of Molecular, Cell and Developmental Biology, University of California Los Angeles, 4028 Terasaki Life Sciences Building, 610 Charles E. Young Drive East, Los Angeles, California 90095, USA [2] Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research, University of California Los Angeles, 615 Charles E. Young Drive South, Los Angeles, California 90095, USA [3] Howard Hughes Medical Institute, University of California Los Angeles, 675 Charles E. Young Drive South, Los Angeles, California 90095, USA.

Published: December 2014

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Article 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.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4268658PMC
http://dx.doi.org/10.1038/ncomms6795DOI Listing

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