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Science. 2016 Nov 18;354(6314):909-912.

The DNA methyltransferase DNMT3C protects male germ cells from transposon activity.

Author information

1
Institut Curie, PSL Research University, INSERM, CNRS, 75005 Paris, France.
2
Ecole des Mines, 75005 Paris, France.
3
PRC, INRA, CNRS, IFCE, Tours University, 37380 Nouzilly, France.
4
Institut de Génétique et Biologie Moléculaire et Cellulaire, Strasbourg University, 67404 Illkirch, France.
5
Centre National de la Recherche Scientifique, UMR7104, Illkirch, France.
6
Institut National de la Santé et de la Recherche Médicale, U964, Illkirch, France.
7
Institut Curie, PSL Research University, INSERM, CNRS, 75005 Paris, France. deborah.bourchis@curie.fr.

Abstract

DNA methylation is prevalent in mammalian genomes and plays a central role in the epigenetic control of development. The mammalian DNA methylation machinery is thought to be composed of three DNA methyltransferase enzymes (DNMT1, DNMT3A, and DNMT3B) and one cofactor (DNMT3L). Here, we describe the discovery of Dnmt3C, a de novo DNA methyltransferase gene that evolved via a duplication of Dnmt3B in rodent genomes and was previously annotated as a pseudogene. We show that DNMT3C is the enzyme responsible for methylating the promoters of evolutionarily young retrotransposons in the male germ line and that this specialized activity is required for mouse fertility. DNMT3C reveals the plasticity of the mammalian DNA methylation system and expands the scope of the mechanisms involved in the epigenetic control of retrotransposons.

PMID:
27856912
DOI:
10.1126/science.aah5143
[Indexed for MEDLINE]

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