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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE60160 | GEO | 2016/06/02

SECONDARY ACCESSION(S): PRJNA257650

REPOSITORIES: GEO

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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

2016-06-02 | E-GEOD-60160 | biostudies-arrayexpress

Expression data from wildtype and Dicer-deficient mouse embryonic stem (ES) cells at different stages of the cell cycle.

2016-06-02 | GSE60096 | GEO

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

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

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

Expression data from wildtype and Dicer-deficient mouse embryonic stem (ES) cells at different stages of the cell cycle.

Project description:The protein Dicer is required for microRNA (miRNA) biogenesis. Dicer-deficient cells therefore lack almost all mature, functional miRNAs. We investigated the role of miRNAs in regulation of gene expression in mouse ES cells by analysing gene expression in either wildtype or Dicer-deficient cells grown either under asynchronous growth conditions, or cells in the early G1 phase of the cell cycle. RNA was extracted from three biological replicates of both wildtype and Dicer-deficient ES cells grown under asynchronous culture conditions. To obtain cells in early G1, populations (in triplicate for both cell types) were cultured in 20ng/ml demecolcine for 4 hours, then mitotic cells were isolated using the mitotic shake-off technique (Terasima & Tolmach, Experimental Cell Research (30) 1963). Mitotic cells were replated in demecolcine-free media for 2 hours, allowing them to progress in a highly synchronised manner into early G1.

2016-06-02 | E-GEOD-60096 | biostudies-arrayexpress

MicroRNAs maintain bivalency in mouse embryonic stem cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2016-06-02 | GSE60161 | GEO

Mapping polycomb complexes in human and mouse embryonic stem cells

Project description:In embryonic stem (ES) cells, bivalent chromatin domains with overlapping repressive (H3 lysine 27 tri-methylation) and activating (H3 lysine 4 tri-methylation) histone modifications mark the promoters of more than 2000 genes. To gain insight into the structure and function of bivalent domains, we mapped key histone modifications and subunits of Polycomb repressive complexes 1 and 2 (PRC1 and PRC2) genomewide in human and mouse ES cells by chromatin immunoprecipitation followed by ultra high-throughput sequencing. We find that bivalent domains can be segregated into two classes: the first occupied by both PRC2 and PRC1 (PRC1-positive) and the second specifically bound by PRC2 (PRC2-only). PRC1-positive bivalent domains appear functionally distinct as they more efficiently retain lysine 27 tri-methylation upon differentiation, show stringent conservation of chromatin state, and associate with an overwhelming number of developmental regulator gene promoters. We also used computational genomics to search for sequence determinants of Polycomb binding. This analysis revealed that the genomewide locations of PRC2 and PRC1 can be largely predicted from the locations, sizes and underlying motif contents of CpG islands. We propose that large CpG islands depleted of activating motifs confer epigenetic memory by recruiting the full repertoire of Polycomb complexes. Keywords: cell type comparison Suz12, Ezh2, Ring1b ChIP-Seq in singlicate from mouse embryonic stem (mES) cells. H3K4me3, H3K27me3, H3K36me3, Ezh2 and Ring1b ChIP-Seq in singlicate from human embyonic stem cells (hES; H9).

2008-11-01 | E-GEOD-13084 | biostudies-arrayexpress

RNA-sequencing analysis of differentiating wildtype and Ezh2 deficient immature mouse chondrocytes

Project description:Objective: To evalute the role of Ezh2 in chondrocyte differentiation. Method: Ezh2 was inactivated in chondrocytes using the Col2a1-Cre driver in vivo. Immature mouse chondrocytes (IMC) were isolated from wildtype and Ezh2 deficient mice, and plated in micromass culture. Chondrocytes were differentiated and RNA was isolated at days 3, 7, and 14 of culture. Isolated RNA was subjected to RNA sequencing analysis. Results: Ezh2 deficient chondrocytes exhibit enhanced expression of osteogenic genes compared to wildtype cells.

2017-03-29 | GSE97118 | GEO

The helicase domain of Dicer ensures strict processing of evolutionarily optimized microRNAs

Project description:Ribonuclease Dicer generates small RNAs for RNA interference (RNAi) and microRNA (miRNA) pathways. Mammalian Dicer produces miRNAs but its tripartite N-terminal helicase domain inhibits processing of double-stranded RNA for RNAi. Mouse oocytes express Dicer, which enhances RNAi because it lacks the helicase’s proximal subdomain HEL1. Here we show that genetic removal of HEL1 in mice causes embryonic growth retardation, defects in the cardiopulmonary system, and perinatal lethality. HEL1 suppresses biogenesis of mirtrons, a non-canonical low-abundant class of miRNAs, and is required for high-fidelity cleavage and strand selection during biogenesis of canonical miRNAs. Essential is the HEL1 structure, not its helicase activity, because mutations of critical aminoacids do not affect viability or fertility and have minimal impact on miRNA biogenesis. Altogether, HEL1 is a critical structural component of Dicer in its role of a highly conserved structural “mold” that ensures high-fidelity processing and adaptive evolution of mammalian miRNA precursors.

2024-04-10 | GSE243016 | GEO

EZH2 deficient T-cell acute lymphoblastic leukemia is sensitized to CHK1 inhibition through enhanced replication stress

Project description:Loss-of-function mutations of EZH2, the enzymatic component of PRC2, have been associated with poor outcome and chemotherapy resistance in T-cell acute lymphoblastic leukemia (T-ALL). Using isogenic T-ALL cells, with and without CRISPR/Cas9-induced EZH2-inactivating mutations, we performed a cell-based synthetic lethal drug screen. EZH2 deficient cells exhibited increased sensitivity to structurally diverse inhibitors of CHK1, an interaction that could be validated genetically. Furthermore, small molecule inhibition of CHK1 had efficacy in delaying tumor progression in isogenic EZH2 deficient, but not EZH2 wild-type T-ALL cells in vivo, as well as in a primary cell model of PRC2 mutant ALL. Mechanistically, EZH2 deficiency resulted in a gene expression signature of immature T-ALL cells, marked transcriptional upregulation of MYCN, increased replication stress, and enhanced dependency on CHK1 for cell survival. Lastly, we demonstrate this phenotype is mediated through de-repression of a distal PRC2-regulated MYCN enhancer. In conclusion, we highlight a novel and clinically exploitable pathway in high-risk EZH2 mutated T-ALL.

2020-05-31 | GSE147198 | GEO

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