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Polycomb associates genome-wide with a specific RNA polymerase II variant, and regulates metabolic genes in ES cells (ChIP-Seq)

ABSTRACT: Polycomb repressor complexes (PRCs) are important chromatin modifiers fundamentally implicated in pluripotency and cancer. Polycomb silencing in embryonic stem cells (ESCs) can be accompanied by active chromatin and primed RNA polymerase II (RNAPII), but the relationship between PRCs and RNAPII remains unclear at the genome-wide level. We mapped PRC repression markers and four RNAPII states in ESCs using ChIP-seq, and found that PRC-targets exhibit a range of RNAPII variants. Firstly, developmental PRC-targets are bound by unproductive RNAPII (S5p+S7p- S2p-) genome-wide. Sequential ChIP, Ring1B-depletion and genome-wide correlations show that PRCs and RNAPII-S5p physically bind to the same chromatin and functionally synergize. Secondly, we identify a cohort of genes marked by PRC and elongating RNAPII (S5p+S7p+S2p+); they produce mRNA and protein, and their expression increases upon PRC1 knockdown. We show that this novel group of PRC-targets switch between active and PRC-repressed states within the ESC population, and that many have roles in metabolism. **Correction (Mar 14, 2012): Due to curation error, runs for SRX112177 and SRX112179 switched, specifically, Run SRR391034.1 was removed from experiment SRX112177 (GSM850468) and added to experiment SRX112179 (GSM850470) as SRR391034.3 Run SRR391040.1 was removed from experiment SRX112179 (GSM850470) and added to experiment SRX112177 (GSM850468) as SRR391040.3

ORGANISM(S): Mus musculus

PROVIDER: GSE34518 | GEO | 2012/02/01

SECONDARY ACCESSION(S): PRJNA156325

REPOSITORIES: GEO

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Polycomb associates genome-wide with a specific RNA polymerase II variant, and regulates metabolic genes in ES cells (ChIP-Seq)

Project description:Polycomb repressor complexes (PRCs) are important chromatin modifiers fundamentally implicated in pluripotency and cancer. Polycomb silencing in embryonic stem cells (ESCs) can be accompanied by active chromatin and primed RNA polymerase II (RNAPII), but the relationship between PRCs and RNAPII remains unclear at the genome-wide level. We mapped PRC repression markers and four RNAPII states in ESCs using ChIP-seq, and found that PRC-targets exhibit a range of RNAPII variants. Firstly, developmental PRC-targets are bound by unproductive RNAPII (S5p+S7p- S2p-) genome-wide. Sequential ChIP, Ring1B-depletion and genome-wide correlations show that PRCs and RNAPII-S5p physically bind to the same chromatin and functionally synergize. Secondly, we identify a cohort of genes marked by PRC and elongating RNAPII (S5p+S7p+S2p+); they produce mRNA and protein, and their expression increases upon PRC1 knockdown. We show that this novel group of PRC-targets switch between active and PRC-repressed states within the ESC population, and that many have roles in metabolism. **Correction (Mar 14, 2012): Due to curation error, runs for SRX112177 and SRX112179 switched, specifically, Run SRR391034.1 was removed from experiment SRX112177 (GSM850468) and added to experiment SRX112179 (GSM850470) as SRR391034.3 Run SRR391040.1 was removed from experiment SRX112179 (GSM850470) and added to experiment SRX112177 (GSM850468) as SRR391040.3 Examination of 4 different RNAPII modifications (S5p, S7p, 8WG16, S2p), and the histone modifications H2Aub1 and H3K36me3 in mouse ES cells

2012-02-01 | E-GEOD-34518 | biostudies-arrayexpress

ZWC Complex-Mediated SPT5 Phosphorylation Suppresses Divergent Antisense RNA Transcription at the Active Gene Promoters [ChIP-Seq]

Project description:Purpose: The goals of this study are to understand the mechanistic roles of newly identified ZWC chromatin complex on the regulation of transcriptional process in actively transcribed genes. The novel ZWC complex is composed of ZC3H4, WDR82, and casein kinase II (CK2) subunits. Methods: Two biological replicates of ChIP-seq data for ZC3H4, WDR82, CK2, and SPT5 were generated from HEK293 cells. And one replicate of ChIP-seq data for RNAPII, H3K4me3, H3K27me3, and H3K36me3 was generated in HEK293 cells. Two biological replicates of ChIP-seq data were generated for RNAPII, S5p RNAPII, S2p RNAPII, SPT5, H3K4me3, H3K36me3, H3K27me3 after HEK293 cells were treated with control or ZC3H4 siRNAs. Results: The ZWC complex preferentially localizes at TSSs of active genes through the direct interactions of ZC3H4 and WDR82 subunits with S5p RNAPII CTD. ZC3H4 depletion leads to increased divergent antisense transcription. Conclusion: Our study provides evidence that the newly identified ZWC-DSIF axis regulates the direction of transcription during the transition from early to productive elongation

2022-03-28 | GSE186758 | GEO

LncRNA-induced spread of Polycomb controlled by genome architecture, RNA abundance, and CpG island DNA [RNA-Seq]

Project description:Long noncoding RNAs (lncRNAs) cause Polycomb Repressive Complexes (PRCs) to spread over broad regions of the mammalian genome. We report that in mouse trophoblast stem cells, the Kcnq1ot1 and Airn lncRNAs induce PRC-dependent chromatin modifications over multi-megabase domains. Throughout the Airn-targeted domain, extent of PRC-dependent modification correlated with intra-nuclear distance to the Airn locus, pre-existing genome architecture, and the abundance of Airn itself. Specific CpG islands displayed characteristics indicating that they nucleate the spread of PRCs upon exposure to Airn. Chromatin environments surrounding Xist, Airn, and Kcnq1ot1 suggest common mechanisms of PRC engagement and spreading. Our data indicate that lncRNA potency can be tightly linked to lncRNA abundance, and that within lncRNA-targeted domains, PRCs are recruited to CpG islands via lncRNA-independent mechanisms. We propose that CpG islands that autonomously recruit PRCs interact with lncRNAs and their associated proteins through 3-dimensional space to nucleate the spread of PRCs in lncRNA-targeted domains.

2019-06-27 | GSE118401 | GEO

LncRNA-induced spread of Polycomb controlled by genome architecture, RNA abundance, and CpG island DNA [ChIP-Seq]

2019-06-27 | GSE118399 | GEO

LncRNA-induced spread of Polycomb controlled by genome architecture, RNA abundance, and CpG island DNA [RIP-seq]

2019-06-27 | GSE129496 | GEO

Chromatin immunoprecipitation of mouse erythroid tissue with RNAPII-S5P ChIP e4C to identify spatial interactomes of mouse globin genes, using alpha and beta globin genes as baits

Project description:RNAPII-S5P ChIP e4C was performed on mouse erythroid tissue, using the alpha and beta globin genes as baits

2009-12-01 | E-TABM-822 | biostudies-arrayexpress

Frequent switching of Polycomb repressive marks and DNA hypermethylation in the PC3 prostate cancer cell line

Project description:Epigenetic reprogramming is commonly observed in cancer, and is hypothesized to involve multiple mechanisms, including DNA methylation and Polycomb repressive complexes (PRCs). Here we devise a new experimental and analytical strategy using customized high density tiling arrays to investigate coordinated patterns of gene expression, DNA methylation and Polycomb marks which differentiate prostate cancer cells from their normal counterparts. Three major changes in the epigenomic landscape distinguish the two cell types. Developmentally significant genes containing CpG islands which are silenced by PRCs in the normal cells acquire DNA methylation silencing and lose their PRC marks (epigenetic switching). Since these genes are normally silent this switch does not cause de novo repression but might significantly reduce epigenetic plasticity. Two other groups of genes are silenced by either de novo DNA methylation without PRC occupancy (5mC reprogramming) or by de novo PRC occupancy without DNA methylation (PRC reprogramming). Our data suggest that the two silencing mechanisms act in parallel to reprogram the cancer epigenome, and that DNA hypermethylation may replace Polycomb based repression near key regulatory genes, possibly reducing their regulatory plasticity. Profiling 5mC and H3K27m3/Suz12 occupancy in the PC3 cancer line and the PrEC system. Hybridization over a custom array including a representative set of promoters (-2.5 to +1 kb) with variable CpG content levels and variable expression levels in the two cell systems.

2008-08-07 | E-GEOD-12334 | biostudies-arrayexpress

Frequent switching of Polycomb repressive marks and DNA hypermethylation in the PC3 prostate cancer cell line

2008-08-07 | GSE12334 | GEO

Upregulation of the mammalian X chromosome is associated with enhanced transcription initiation, MOF-mediated H4K16 acetylation, and longer RNA half-life

Project description:Many animal species employ a chromosome-based mechanism of sex determination, which has led to coordinate evolution of dosage compensation systems. Dosage compensation not only corrects the imbalance in the number of X-chromosomes between the sexes, but is also hypothesized to correct dosage imbalance within cells due to mono-allelic X expression and bi-allelic autosomal expression, by upregulating X-linked genes (termed ‘Ohno’s hypothesis’). To identify molecular mechanisms of X upregulation in mammals we established genome-wide profiles for the initiation and elongation forms of RNA polymerase II (PolII), PolII-S5p (phosphorylated at serine 5) and PolII-S2p (phosphorylated at serine 2), and for histone modifications in mouse cell lines and tissues. We found that in addition to being enriched in PolII-S5p but not in PolII-S2p, X-linked promoters were also enriched in two epigenetic marks, H4K16ac and H2AZ, dependent on expression levels. To address the function of the H4K16 acetyltransferase MOF occupancy profiles were established and knockdowns of MOF and MSL1 were done in mouse ES cells. Our results support a conserved role for the MSL complex to enhance transcription initiation of X-linked genes.

2013-03-05 | GSE44835 | GEO

Upregulation of the mammalian X chromosome is associated with enhanced transcription initiation, MOF-mediated H4K16 acetylation, and longer RNA half-life

Project description:Many animal species employ a chromosome-based mechanism of sex determination, which has led to coordinate evolution of dosage compensation systems. Dosage compensation not only corrects the imbalance in the number of X-chromosomes between the sexes, but is also hypothesized to correct dosage imbalance within cells due to mono-allelic X expression and bi-allelic autosomal expression, by upregulating X-linked genes (termed M-bM-^@M-^XOhnoM-bM-^@M-^Ys hypothesisM-bM-^@M-^Y). To identify molecular mechanisms of X upregulation in mammals we established genome-wide profiles for the initiation and elongation forms of RNA polymerase II (PolII), PolII-S5p (phosphorylated at serine 5) and PolII-S2p (phosphorylated at serine 2), and for histone modifications in mouse cell lines and tissues. We found that in addition to being enriched in PolII-S5p but not in PolII-S2p, X-linked promoters were also enriched in two epigenetic marks, H4K16ac and H2AZ, dependent on expression levels. To address the function of the H4K16 acetyltransferase MOF occupancy profiles were established and knockdowns of MOF and MSL1 were done in mouse ES cells. Our results support a conserved role for the MSL complex to enhance transcription initiation of X-linked genes. Comparison of the profiles of RNA PolII, the H4K16ac acetyltransferase MOF and histone active marks on the X versus autosomes in mouse

2013-03-05 | E-GEOD-44835 | biostudies-arrayexpress

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