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Mouse ES cells expressing catalytically inactive Ring1B display impaired Ring1B and H3K27me3 deposition.

ABSTRACT: ChIP-seq for H3K27me3 and Ring1B was performed in WT mESCs and mESCs containing catalytically inactive Ring1B (I53A mutant). Cells expressing catalytically inactive Ring1B maintain the spatial distribution of Ring1B and H3K27me3 but at reduced levels. These findings support the notion that PRC2 recruitment is, in part, dependent on H2A ubiquitination (H2AK119ub).

ORGANISM(S): Mus musculus

PROVIDER: GSE69955 | GEO | 2015/09/20

SECONDARY ACCESSION(S): PRJNA287271

REPOSITORIES: GEO

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Mouse ES cells expressing catalytically inactive Ring1B display impaired Ring1B and H3K27me3 deposition.

Project description:ChIP-seq for H3K27me3 and Ring1B was performed in WT mESCs and mESCs containing catalytically inactive Ring1B (I53A mutant). Cells expressing catalytically inactive Ring1B maintain the spatial distribution of Ring1B and H3K27me3 but at reduced levels. These findings support the notion that PRC2 recruitment is, in part, dependent on H2A ubiquitination (H2AK119ub). Two biological replicates were performed for Ring1B and H3K27me3 ChIPs in WT and Ring1B I53A/I53A mouse ESCs. Input chromatin was sequenced for each replicate as a control for ChIP enrichment.

2015-09-20 | E-GEOD-69955 | biostudies-arrayexpress

Catalytically inactive Ring1B maintains near wildtype levels of gene expression in mESCs

Project description:This experiment was designed to determine the extent of gene misregulation in mESCs containing catalytically dead Ring1B in comparison to mESCs lacking Ring1B. Polyadenylated mRNA was prepared from wildtype mESCs (WT), mESCs deficient for Ring1B (KO) and mESCs cells containing catalytically dead Ring1B (I53A). Each sample is represented by 3 biological replicate hybridisations.

2015-09-20 | E-GEOD-69824 | biostudies-arrayexpress

Catalytically inactive Ring1B maintains near wildtype levels of gene expression in mESCs

Project description:This experiment was designed to determine the extent of gene misregulation in mESCs containing catalytically dead Ring1B in comparison to mESCs lacking Ring1B.

2015-09-20 | GSE69824 | GEO

Functional Dissection of Variant Polycomb Repressive Complex 1 Subunits RYBP and YAF2 during Neural Differentiation of Embryonic Stem Cells [ChIP-Seq]

Project description:Chromatin immunoprecipitation sequencing (ChIP-seq) for RING1B, RYBP, YAF2, PRC2 complex (EZH2, MTF2 and JARID2) as well as the histone modifications H2AK119ub, H3K27me3 and H3K27ac in mESCs and the neural differentiated cells.

2023-10-09 | GSE213414 | GEO

Mus musculus

Project description:Mouse ES cells expressing catalytically inactive Ring1B display impaired Ring1B and H3K27me3 deposition.

| PRJNA287271 | ENA

Mus musculus

Project description:Catalytically inactive Ring1B maintains near wildtype levels of gene expression in mESCs

| PRJNA286873 | ENA

Transcriptome profile of oocytes expressing a catalytically inactive knock-in allele of Ago2

Project description:The RNase III enzyme DICER generates both microRNAs (miRNAs) and endogenous short interfering RNAs (endo-siRNAs). Dicer deletion in mouse oocytes leads to female infertility due to defects during meiosis I. Because miRNA function is suppressed in mouse oocytes, it has been proposed that endo-siRNAs may have a role during female meiosis. By utilizing a catalytically inactive knock-in allele of AGO2 specifically in oocytes, we disrupt the function of siRNAs and analyze the transcriptome of these oocytes in comparison with Ago2 null, and Dicer null oocytes. Germinal vesicle-intact, full-grown oocytes were collected from eCG-primed females expressing a catalytically inactive knock-in allele of Ago2 (Ago2 ADH) specifically in oocytes. Oocytes were also collected from Ago2 null and Ago2 fl/fl oocytes, as well as Dicer wild-type and null mice. Oocytes were freed of attached cumulus cells by pipetting. Twenty oocytes collected from 3 different mice were used for high-throughput RNA sequencing. Three replicates for all genotypes except Ago2 null (two). The mouse background strain is "mostly" C57BL6, i.e., it is a cross between 3 different transgenic mice of different strains.

2015-01-20 | E-GEOD-57514 | biostudies-arrayexpress

Transcriptome profile of oocytes expressing a catalytically inactive knock-in allele of Ago2

2015-01-20 | GSE57514 | GEO

Genome-wide profiling of transcription, H3K27me3 and RING1B occupancy in mouse ESCs following EZH1/2 inhibition

Project description:Mouse embryonic stem cells (mESCs) were treated with DMSO (control) or EPZ-6438 (EPZ; a potent inhibitor of the EZH1/2) for 24 h. ChIP-seq was used to determine the impact of this treatment on the level and distribution of H3K27me3 and RING1B genome-wide. In parallel, gene expression was assessed by deep sequencing of both total RNA (RNA-seq) and 4-thiouridine metabolically labelled RNA (4sU-seq). Calibrated ChIP-seq, utilizing Drosophila chromatin as an exogenous control, demonstrated a marked global depletion of H3K27me3 following 24 h of EPZ treatment concomitant with a substantial reduction in RING1B occupancy. A rather modest change in the levels of total and nascent transcripts allowed us to identify a direct contribution of the polycomb system in controlling chromatin architecture and 3D nuclear organization.

2019-12-15 | GSE140894 | GEO

Chip-chip from Mouse E10.5 anterior and posterior immortalised limb cell lines and limb tissue for H3K27me3 antibody and from Mouse E10.5 anterior and posterior limb tissue for Ring1B antibody.

Project description:Anterior-posterior differences in H3K27me3 and Ring1B enrichment over the 5 prime Hoxd genes in E10.5 murine distal forelimbs. Chromatin immunoprecipitation (ChIP) of H3K27me3 together with Ring1B and by ChIP-on-chip analysis demonstrated that over the 5 prime HoxD locus H3K27me3 enrichment is decreased and Ring1B enrichment is sparse in limb cells derived from the distal posterior forelimb bud of E10.5 mouse embryos.

2012-09-18 | GSE38526 | GEO

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