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ABSTRACT: Loss of Ring1B catalytic activity causes a pronounced reduction in H3K27me3 deposition yet minimally disrupts the expression of target genes

OTHER RELATED OMICS DATASETS IN: GSE69978

PROVIDER: PRJNA287319 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR2067630.fastq.gz	Fastqsanger.gz
	SRR2067631.fastq.gz	Fastqsanger.gz
	SRR2067632.fastq.gz	Fastqsanger.gz
	SRR2067633.fastq.gz	Fastqsanger.gz
	SRR2067624.fastq.gz	Fastqsanger.gz

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Histone H2AK119 Mono-Ubiquitination is Essential for Polycomb-Mediated Transcriptional Repression

Project description:The major function of Polycomb group proteins (PcG) is to maintain transcriptional repression to preserve cellular identity. This is exerted by two distinct repressive complexes, PRC1 and PRC2, that modify histones by depositing H2AK119ub1 and H3K27me3, respectively. Both complexes are essential for development and are deregulated in several types of human tumors. PRC1 and PRC2 exist in different variants and show a complex regulatory cross-talk. However, the contribution that H2AK119ub1 plays in mediating PcG repressive functions remains largely controversial. Coupling an inducible system with the expression of a fully catalytic inactive RING1B mutant, we demonstrated that H2AK119ub1 deposition is essential to maintain PcG-target genes repressed in ESC. Loss of H2AK119ub1 induced a rapid displacement of PRC2 activity and a loss of H3K27me3 deposition. This affected both PRC2.1 and PRC2.2 variants and further correlated with a strong displacement and destabilization of canonical PRC1. Finally, we find that variant PRC1 forms can sense H2AK119ub1 deposition, which contributes to their stabilization specifically at sites where this modification is highly enriched. Overall our data place H2AK119ub1 deposition as central hub that mount PcG repressive machineries to preserve cell transcriptional identit

2019-12-26 | GSE134053 | GEO

Mus musculus

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

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

2015-09-20 | GSE69955 | GEO

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

A Central Role for PRC1 in Shaping the 3D Nuclear Landscape

Project description:1. Loss of RING1B substantially disrupts nuclear architecture. 2. PRC1 mediated looping can occur at a Mb scale and is independent of CTCF. 3. Polycomb mediated looping is driven by canonical PRC1 complexes. 4. Trimeric PRC1-mediated interactions occur in vitro and in vivo. 5. Gene up-regulation does not directly lead to the loss of PRC1 loops.

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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.

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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. Array design includes 2 biological replicates for H3K27me3 in the cell lines and Ring1B in the limb tissue, and 2 biological replicates and 2 dye swap replicates for H3K27me3 in the limb tissue.

2012-09-18 | E-GEOD-38526 | biostudies-arrayexpress

ChIP-seq for Polycomb group proteins and H3K27me3 in ESCs and NSCs

Project description:ChIP-seq was performed for Ring1b, Ezh2, Cbx2 and H3K27me3 in ESCs and Ring1b and H3K27me3 in NSCs. This was used to define Polycomb-bound regions and to assess their H3.3 enrichment and turnover using time-ChIP.

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Genome-wide profiling of trimethylated histone H3 lysine 27 (H3K27me3) in wide-type, brm, clf, and brm clf mutant seedlings

Project description:By using ChIP-seq, we found that loss of BRM activity in developing seedlings leads to ectopic and increased H3K27me3 deposition at several hundred genes, indicating the critical role of BRM in preventing the inappropriate deposition of this histone mark. Removal of CLF in brm mutant could partcially suppress the increased H3K27me3. Examination of H3K27me3 in 14-day-old wt, brm, clf, and brm clf seedlings. Two biological replicates for each one.

2015-03-09 | E-GEOD-53620 | biostudies-arrayexpress

Genome-wide profiling of trimethylated histone H3 lysine 27 (H3K27me3) in brm mutant seedlings and in wt seedlings

Project description:By using ChIP-seq, we found that loss of BRM activity in developing seedlings leads to ectopic and increased H3K27me3 deposition at several hundred genes, indicating the critical role of BRM in preventing the inappropriate deposition of this histone mark. Unexpectedly, BRM also facilitates PcG function at some PcG targets, suggesting the requirement for BRM in the deposition of this mark at certain PcG target genes. Examination of H3K27me3 in 14-day-old wt and brm seedlings. Two biological replicates for each one.

2014-03-01 | E-GEOD-47202 | biostudies-arrayexpress

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