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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE78899 | GEO | 2016/06/20

SECONDARY ACCESSION(S): PRJNA314337

REPOSITORIES: GEO

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Time-ChIP in ESCs and NSCs

Project description:Histone H3.3 turnover in ESCs and NSCs was determined using time-ChIP. This was performed by biotin-labeling H3.3_SNAP and following the loss of labeled histones over time. H3.1 time-ChIP was also performed although the resolution of these data is limited due to the depth of sequencing required.

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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.

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

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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.

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Project description:Polycomb proteins are classical regulators of stem cell self-renewal and cell lineage commitment and are frequently deregulated in cancer. Here we find that the non-canonical PRC1.1 complex, as identified by mass spectrometry-based proteomics, is critically important for human leukemic stem cells. Downmodulation of PRC1.1 complex members, like the DNA-binding subunit KDM2B, strongly reduces cell proliferation in vitro and delays or even abrogates leukemogenesis in vivo in humanized xenograft models. PRC1.1 components are significantly overexpressed in primary AML CD34+ cells. Besides a set of genes that is co-targeted by PRC1 and PRC2, ChIP-seq studies show that PRC1.1 also binds a distinct set of genes that are devoid of H3K27me3 suggesting a gene regulatory role independent of PRC2. This set encompasses genes involved in metabolism, which have transcriptionally active chromatin profiles. These data indicate that PRC1.1 controls distinct gene clusters involved in unique cell biological processes required for leukemic cell viability. K562 cells were transduced with lentiviral GFP-fusion vectors encoding GFP-CBX2, PCGF1-GPF, PCGF2-GFP, PCGF4-GFP, GFP-RING1A or GFP-RING1B. K562 cells expressing GFP-fusions at relatively low levels were sorted and expanded and subsequently crosslinked. ChIP reactions were performed using the following antibodies: anti-GFP (ab290, Abcam), anti-H3K27me3 (07-449, Millipore), anti-H3K4me3 (ab8580, Abcam), anti-H2AK119ub (D27C4, Cell Signaling Technology), and anti-KDM2B (ab137547, Abcam). Furthermore, ChIP reactions were performed using primary AML CD34+ and Peripheral Blood (PB) CD34+ cells using anti-H3K27me3 (07-449, Millipore), anti-H3K4me3 (ab8580, Abcam), anti-H2AK119ub (D27C4, Cell Signaling Technology), anti-KDM2B (ab137547, Abcam).

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