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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. Examination of Ezh2 binding in mouse ES cells either proficient (wildtype) or deficient (KO) of the protein Dicer

ORGANISM(S): Mus musculus

SUBMITTER: Gopuraja Dharmalingam

PROVIDER: E-GEOD-60160 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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

Graham Bryony B Marcais Antoine A Dharmalingam Gopuraja G Carroll Thomas T Kanellopoulou Chryssa C Graumann Johannes J Nesterova Tatyana B TB Bermange Anna A Brazauskas Pijus P Xella Barbara B Kriaucionis Skirmantas S Higgs Douglas R DR Brockdorff Neil N Mann Matthias M Fisher Amanda G AG Merkenschlager Matthias M

Stem cell reports 20160414 5

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 ...[more]

PMID: 27150236

Similar Datasets

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 [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.

2016-06-02 | GSE60160 | GEO

Dicer deficiency reveals microRNAs predicted to control gene expression in developing adrenal cortex [array]

Project description:MicroRNAs (miRNAs) are small, endogenous, non-protein coding RNAs that are an important means of post-transcriptional gene regulation. Deletion of Dicer, a key miRNA processing enzyme, is embryonic lethal in mice, and tissue-specific Dicer deletion results in developmental defects. Using a conditional knockout model, we generated mice lacking Dicer in the adrenal cortex. These Dicer knockout (KO) mice exhibited perinatal mortality and failure of the adrenal cortex during late gestation between embryonic day 16.5 (E16.5) and E18.5. Further study of Dicer KO adrenals demonstrated a significant loss of Sf1 expressing cortical cells that was histologically evident as early as E16.5 coincident with an increase in p21 and cleaved-caspase 3 staining in the cortex. However, peripheral cortical proliferation persisted in KO adrenals as assessed by anti-PCNA staining. To further characterize the embryonic adrenals from Dicer KO mice, we performed microarray analyses for both gene expression and miRNA on purified RNA isolated from control and KO adrenals of E15.5 and E16.5 embryos. Consistent with the absence of Dicer and the associated loss of miRNA-mediated mRNA degradation, we observed an up-regulation of a small subset of adrenal transcripts in Dicer KO mice, most notably the transcripts coded by the genes Nr6a1 and Acvr1c. Indeed, several miRNAs, including let-7, miR-34c, and miR-21 that are predicted to target these genes for degradation, were also markedly down-regulated in Dicer KO adrenals. Together these data suggest a role for miRNA mediated regulation of a subset of genes that are essential for normal adrenal growth and homeostasis. Adrenals from control and Dicer KO litter mates were pooled separately from 4 individual litters, resulting in a total of 4 control (cre-) and 4 Dicer KO biological replicates at both E15.5 and E16.5.

2013-05-01 | E-GEOD-45592 | biostudies-arrayexpress

Dicer deficiency reveals microRNAs predicted to control gene expression in developing adrenal cortex [RT-PCR]

2013-05-01 | E-GEOD-45810 | biostudies-arrayexpress

DICER controls macrophage polarization and tumor response to immunotherapy

Project description:Tumor-associated macrophages (TAMs) have immunosuppressive capacity in mouse models of cancer. Here we show that the genetic deletion of the microRNA (miRNA)-processing enzyme DICER in TAMs broadly programs them to a CD11c+MRC1â/low M1-like immunostimulatory phenotype characterized by activated interferon-Î³ (IFN-Î³)/STAT1/IRF signaling. M1-like TAM programming fostered the recruitment of cytotoxic T-cells (CTLs), including tumor-antigen-specific CTLs, inhibited tumor growth, and enhanced the efficacy of PD1 checkpoint blockade. Bioinformatics analysis of TAM transcriptomes identified a limited set of miRNAs putatively involved in TAM programming. Re-expression of Let-7 in Dicer-deficient TAMs was sufficient to partly rescue the M2-like (protumoral) TAM phenotype and abate tumor CTL infiltration. Targeted suppression of DICER activity in TAMs may, therefore, stimulate antitumor immunity and enhance the efficacy of cancer immunotherapy. To explore the role of DICER in the development, activation and immunological functions of TAMs, we crossed homozygous LysM-Cre (Clausen et al., 1999) with Dicerlox/lox (Harfe et al., 2005) mice to obtain mice with myeloid-cell-specific Dicer1 gene deletion (LysM-Cre;Dicerâ/â, referred to as Dâ/â). These mice were then backcrossed to LysM-Cre to obtain the control LysM-Cre; Dicer+/+ mice (referred to as D+/+). Both LysM-Cre and Dicerlox/lox mutations were always homozygous in our experiment. We then inoculated Lewis lung carcinoma (LLC) cells subcutaneously (s.c.) in Dâ/â and control D+/+ mice. Once the tumors were established, we isolated by fluorescence-activated cell sorting (FACS) tumor-associated macrophages (F4/80+ cells).

2016-06-13 | E-GEOD-76356 | biostudies-arrayexpress

The effects of the 5' pocket motif of Dicer on miRNA biogenesis

Project description:A hallmark of RNA silencing is a class of ~22 nt RNAs which are processed from dsRNA precursor by Dicer. Accurate processing by Dicer is critical for the functionality of microRNAs (miRNAs). According to the current model, Dicer measures the length by anchoring the 3' overhang of the dsRNA terminus. Here we find that human Dicer binds to the 5' end of RNA and utilizes the 5' end as an additional reference point for cleavage site selection (5' counting rule). We further identify a novel motif (5'-pocket) in Dicer, which recognizes the 5' end of RNA. By analyzing miRNA population from 5'-pocket mutant Dicer expressing Dicer-null mES, we provide that the 5' pocket is significant for Dicer processing in vivo. Examination of small RNA profiles from Dicer-null mouse embryonic stem cells transfected with either wild-type or 5' pocket mutant Dice expression plasmids.

2011-07-12 | E-GEOD-27903 | biostudies-arrayexpress

Comprehensive gene expression changes by the expression levels of Dicer protein

Project description:MicroRNA regulates gene expression. In this experiment, we determined the gene expression changes by the microRNA expression status using Dicer protein nulll. Wildtype, and intermediate expression. Dicer gene disrupted HCT116 colon cancer cells were transduced with tetracycline regulated Dicer protein expression. To determine the gene expression changes dependent on the Dicer protein levels, we used Dicer disrupted cells, Dicer wild-type cells, and cells with intermediate expression level of Dicer protein for the cDNA microarrya analyses.

2016-08-23 | E-GEOD-85909 | biostudies-arrayexpress

Endogenous shRNAs, siRNAs, and Other Microprocessor-independent, Dicer-dependent Small RNAs in Mouse ES Cells

Project description:Canonical microRNAs (miRNAs) require two processing steps: the first by the Microprocessor, a complex of DGCR8 and Drosha, and the second by Dicer. dgcr8delta/delta mouse embryonic stem cells (mESCs) have less severe phenotypes than dicer1delta/delta mESCs, suggesting a physiological role for Microprocessor-independent, Dicer-dependent small RNAs. To identify these small RNAs with unusual biogenesis, we performed high-throughput sequencing from wild type, dgcr8delta/delta, and dicer1delta/delta mESCs. Several of the DGCR8-independent, Dicer-dependent RNAs were non-canonical miRNAs. These derived from mirtrons and a newly identified subclass of miRNA precursors, which appears to be the endogenous counterpart of short hairpin RNAs (shRNAs). Our analyses also revealed endogenous siRNAs resulting from Dicer cleavage of long hairpins, the vast majority of which originated from one genomic locus with tandem, inverted short interspersed nuclear elements (SINEs). Our results extend the known diversity of mammalian small-RNA generating pathways and show that mammalian siRNAs exist in tissues outside of oocytes. Small RNAs were sequenced from wt, dgcr8(-), and dicer(-) mouse ES cells and the frequencies of small RNA types compared between the three. This record includes Illumina-platform-generated datasets from all three samples and 454-platform-generated datasets from wt and dgcr8(-) samples. [raw data files are unavailable]

2008-09-09 | E-GEOD-12521 | biostudies-arrayexpress

Gene expression profile of Dicer-deficient oocytes

Project description:Small RNAs, such as miRNAs and siRNAs, are involved in gene regulation in a variety of systems, including mouse oocytes. Dicer is a ribonuclease III enzyme essential for miRNA and siRNA biosynthesis. In an effort to uncover the function of small RNAs during oocyte growth, we specifically deleted Dicer in growing oocytes and analyzed the global pattern of gene expression in these Dicer-deficient oocytes. Germinal vesicle-intact, fully grown oocytes were collected from eCG-primed wild-type or Dicer-deficient female mice and freed of attached cumulus cells by pipetting. Twenty oocytes per mouse were used for RNA extraction and hybridization on the MOE430 v2 Affymetrix microarray platform. Oocytes from four wild-type and four Dicer-knockout mice were analyzed.

2010-04-06 | E-GEOD-17985 | biostudies-arrayexpress

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