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PRC1 and Suv39h specify parental asymmetry at constitutive heterochromatin in early mouse embryos.

Puschendorf, Mareike and Terranova, Remi and Boutsma, Erwin and Mao, Xiaohong and Isono, Kyo-ichi and Brykczynska, Urszula and Kolb, Carolin and Otte, Arie P and Koseki, Haruhiko and Orkin, Stuart H and van Lohuizen, Maarten and Peters, Antoine (2008) PRC1 and Suv39h specify parental asymmetry at constitutive heterochromatin in early mouse embryos. Nature Genetics, 40 (4). pp. 411-420. ISSN 1546-1718

Abstract

In eukaryotes, Suv39h H3K9 trimethyltransferases are required for pericentric heterochromatin formation and function. In early mouse preimplantation embryos, however, paternal pericentric heterochromatin lacks Suv39h-mediated H3K9me3 and downstream marks. Here we demonstrate Ezh2-independent targeting of maternally provided polycomb repressive complex 1 (PRC1) components to paternal heterochromatin. In Suv39h2 maternally deficient zygotes, PRC1 also associates with maternal heterochromatin lacking H3K9me3, thereby revealing hierarchy between repressive pathways. In Rnf2 maternally deficient zygotes, the PRC1 complex is disrupted, and levels of pericentric major satellite transcripts are increased at the paternal but not the maternal genome. We conclude that in early embryos, Suv39h-mediated H3K9me3 constitutes the dominant maternal transgenerational signal for pericentric heterochromatin formation. In absence of this signal, PRC1 functions as the default repressive back-up mechanism. Parental epigenetic asymmetry, also observed along cleavage chromosomes, is resolved by the end of the 8-cell stage--concurrent with blastomere polarization--marking the end of the maternal-to-embryonic transition.

Item Type: Article
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Additional Information: author can archive post-print (ie final draft post-refereeing); Publisher's version/PDF cannot be used
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Date Deposited: 14 Dec 2009 13:52
Last Modified: 31 Jan 2013 01:04
URI: https://oak.novartis.com/id/eprint/873

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