Polycomb group proteins Ezh2 and Rnf2 direct genomic contraction and imprinted repression in early mouse embryos

Genomic imprinting regulates parental-specific expression of particular genes and is required for normal mammalian development. How imprinting is established during development is, however, largely unknown. To address this question, we studied the mouse Kcnq1 imprinted cluster at which paternal-spec...

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Podrobná bibliografie
Vydáno v:	Developmental cell Ročník 15; číslo 5; s. 668
Hlavní autoři:	Terranova, Rémi, Yokobayashi, Shihori, Stadler, Michael B, Otte, Arie P, van Lohuizen, Maarten, Orkin, Stuart H, Peters, Antoine H F M
Médium:	Journal Article
Jazyk:	angličtina
Vydáno:	United States 01.11.2008
Témata:	Animals Cell Nucleus - genetics Cell Nucleus - metabolism Chromatin Assembly and Disassembly DNA-Binding Proteins - metabolism Embryo, Mammalian - metabolism Enhancer of Zeste Homolog 2 Protein Female Genomic Imprinting Histone-Lysine N-Methyltransferase - metabolism Male Mice Polycomb Repressive Complex 1 Polycomb Repressive Complex 2 Repressor Proteins - metabolism RNA, Long Noncoding RNA, Untranslated - metabolism Ubiquitin-Protein Ligases - metabolism
ISSN:	1878-1551, 1878-1551
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Popis
Shrnutí:	Genomic imprinting regulates parental-specific expression of particular genes and is required for normal mammalian development. How imprinting is established during development is, however, largely unknown. To address this question, we studied the mouse Kcnq1 imprinted cluster at which paternal-specific silencing depends on expression of the noncoding RNA Kcnq1ot1. We show that Kcnq1ot1 is expressed from the zygote stage onward and rapidly associates with chromatin marked by Polycomb group (PcG) proteins and repressive histone modifications, forming a discrete repressive nuclear compartment devoid of RNA polymerase II, a configuration also observed at the Igf2r imprinted cluster. In this compartment, the paternal Kcnq1 cluster exists in a three-dimensionally contracted state. In vivo the PcG proteins Ezh2 and Rnf2 are independently required for genomic contraction and imprinted silencing. We propose that the formation of a parental-specific higher-order chromatin organization renders imprint clusters competent for monoallelic silencing and assign a central role to PcG proteins in this process.
Bibliografie:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
ISSN:	1878-1551 1878-1551
DOI:	10.1016/j.devcel.2008.08.015