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MicroRNAs maintain bivalency in mouse embryonic stem cells

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE60161 | GEO | 2016/06/02

SECONDARY ACCESSION(S): PRJNA257647

REPOSITORIES: GEO

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MicroRNAs maintain bivalency in mouse embryonic stem cells

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2016-06-02 | E-GEOD-60161 | biostudies-arrayexpress

MicroRNAs of the miR-290-295 Family Maintain Bivalency in Mouse Embryonic Stem Cells.

Project description:Numerous developmentally regulated genes in mouse embryonic stem cells (ESCs) are marked by both active (H3K4me3)- and polycomb group (PcG)-mediated repressive (H3K27me3) histone modifications. This bivalent state is thought to be important for transcriptional poising, but the mechanisms that regulate bivalent genes and the bivalent state remain incompletely understood. Examining the contribution of microRNAs (miRNAs) to the regulation of bivalent genes, we found that the miRNA biogenesis enzyme DICER was required for the binding of the PRC2 core components EZH2 and SUZ12, and for the presence of the PRC2-mediated histone modification H3K27me3 at many bivalent genes. Genes that lost bivalency were preferentially upregulated at the mRNA and protein levels. Finally, reconstituting Dicer-deficient ESCs with ESC miRNAs restored bivalent gene repression and PRC2 binding at formerly bivalent genes. Therefore, miRNAs regulate bivalent genes and the bivalent state itself.

| S-EPMC4939759 | biostudies-literature

MicroRNAs maintain bivalency in mouse embryonic stem cells [ChIP-seq]

Project description:The protein Dicer is required for microRNA (miRNA) biogenesis, and therefore Dicer-deficient cells lack all mature, functional miRNAs. Here we investigated the binding of the PRC2 component Ezh2 in wildtype and Dicer-deficient mouse embryonic stem cells genomewide using ChIP-sequencing analysis. Examination of Ezh2 binding in mouse ES cells either proficient (wildtype) or deficient (KO) of the protein Dicer

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