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Mapping early PRC2 nucleation sites upon Suz12 reintroduction reveals features of de novo Polycomb recruitment [ChIP-seq]

ABSTRACT: Polycomb domains safeguard cell identity by maintaining lineage-specific chromatin states enriched in repressive histone modifications preserving the epigenetic memory of each cell lineage. While Polycomb Repressive Complex 2 (PRC2) can re-establish its occupancy after perturbation, the mechanisms that guide de novo Poly-comb recruitment remain unclear. To address this, we engineered an auxin-inducible degradation system to reversibly deplete and reintroduce the endogenous PRC2 core subunit Suz12 in mouse embryonic stem cells (mESCs). Genome-wide profiling at early recovery time point revealed PRC2 nucleation sites, characterized by rapid Suz12 and H3K27me3 re-accumulation and signal strength.

ORGANISM(S): Mus musculus

PROVIDER: GSE305054 | GEO | 2026/02/25

REPOSITORIES: GEO

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Mapping early PRC2 nucleation sites upon Suz12 reintroduction reveals features of de novo Polycomb recruitment [RNA-seq]

Project description:Polycomb domains safeguard cell identity by maintaining lineage-specific chromatin states enriched in repressive histone modifications preserving the epigenetic memory of each cell lineage. While Polycomb Repressive Complex 2 (PRC2) can re-establish its occupancy after perturbation, the mechanisms that guide de novo Poly-comb recruitment remain unclear. To address this, we engineered an auxin-inducible degradation system to reversibly deplete and reintroduce the endogenous PRC2 core subunit Suz12 in mouse embryonic stem cells (mESCs). Genome-wide profiling at early recovery time point revealed PRC2 nucleation sites, characterized by rapid Suz12 and H3K27me3 re-accumulation and signal strength.

2026-02-25 | GSE305055 | GEO

The Polycomb Group Protein Suz12 Is Required for Embryonic Stem Cell Differentiation

2011-08-12 | GSE31354 | GEO

The Polycomb Group Protein Suz12 Is Required for Embryonic Stem Cell Differentiation

Project description:Polycomb group (PcG) proteins form multiprotein complexes, called Polycomb repressive complexes (PRCs). PRC2 contains the PcG proteins EZH2, SUZ12, and EED and represses transcription through methylation of lysine (K) 27 of histone H3 (H3). Suz12 is essential for PRC2 activity and its inactivation results in early lethality of mouse embryos. Total RNA was extracted independently from three WT and three Suz12 KO ES cell clones. RNA was quantified, and equal amounts fromthe three Suz12 WT and the three Suz12 KO samples were pooled into one sample to reduce the experimental variation. Targets for microarray hybridization were synthesized according to the supplier’s instructions (Affymetrix). Hybridization, washing, staining, scanning, and data analysis were performed at the Affymetrix microarray unit at the Institute of Molecular Oncology of the Italian Foundation for Cancer Research-European Institute of Oncology campus, Milan, Italy, according to the manufacturer’s instructions.

2011-08-11 | E-GEOD-31354 | biostudies-arrayexpress

JAZF1-SUZ12 dysregulates PRC2 recruitment and gene expression during cell differentiation

Project description:Polycomb repressive complex 2 (PRC2) maintains repression of genes specific for other cell differentiation stages through methylation of histone H3 lysine 27 (H3K27me3) and is regulated by nascent RNA. In endometrial stromal sarcoma, the PRC2 subunit SUZ12 is often fused with the transcription factor JAZF1. How JAZF1-SUZ12 affects PRC2 function and cell differentiation are unknown. Here, we show that JAZF1-SUZ12 disrupts PRC2 recruitment, gene expression and cell differentiation. The loss of the SUZ12 N-terminus in the fusion protein disrupted interaction with JARID2, EPOP and PALI1 and prevented recruitment of PRC2 from RNA to chromatin. JAZF1-SUZ12 occupied PRC2 target genes in undifferentiated cells but relocated to JAZF1 target genes during cell differentiation, altering patterns of H3K27me3 and gene expression and disrupting cell differentiation. We then performed RNA-seq in primary human cells expreesing all proteins, showing that JAZF1-SUZ12 was promoting a specific set of genes upregulated in decidualisation, while blocking immune related genes. These results reveal the defects in PRC2 function and cell differentiation caused by the JAZF1-SUZ12 fusion protein, which may underlie its role in oncogenesis.

2022-04-25 | GSE169658 | GEO

H3K27me3 is maintained at a reduced level in Suz12(Bgal/Bgal) ESCs [ChIP-Seq]

Project description:Suz12(Bgal/Bgal) ESCs express a truncated form of Suz12 fused to Beta-galactosidase. These cells maintain a reduced level of H3K27me3 despite this mutation to a core component of PRC2, unlike Eed-/- ESCs whose H3K27me3 is ablated. Two ESC lines mutant in genes of core components of Polycomb Repressive Complex 2 were assessed for H3K27me3 by ChIP-seq, as compared to a wild type ESC line.

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SUZ12 and NF1 loss cooperate to enhance Ras transcriptional output and sensitize cancers to epigenetic therapies

Project description:The polycomb repressive complex 2 (PRC2) plays an oncogenic role in several cancers. However, loss-of-function mutations in PRC2 components have been detected in a subset of hematopoietic malignancies, suggesting that different epigenetic landscapes are required in different tumor types. In this study we provide genomic, cellular, and mouse modeling data to demonstrate that loss-of-function mutations in the polycomb gene, SUZ12, and NF1 cooperate in peripheral nervous system tumors, glioblastomas, and melanomas. NF1 encodes a Ras GTPase-activating protein and its loss triggers moderate levels of Ras activation. We show that SUZ12-loss enhances the effects of NF1 mutations, in part, by amplifying Ras transcriptional signatures. Moreover, SUZ12-loss triggers an epigenetic switch that confers sensitivity to combined bromodomain and MEK inhibitors in vivo. Collectively these studies demonstrate an unexpected role for polycomb group genes in NF1 mutant tumors and reveal an epigenetic-based therapeutic strategy that may be exploited for a variety of cancers. 9 samples in triplicates, 3x LacZ control, 3x SUZ12 over expression, 3x JQ1 treatment

2014-07-01 | E-GEOD-52777 | biostudies-arrayexpress

SUZ12 immunoprecipitation followed by protein indentification via mass spectrometry (SUZ12 IP-MS) in mESCs of SUZ12 WT, delta exon 4, KO, and KO rescues with SUZ12-L and SUZ12-S

Project description:Suz12 exon 4 encodes 23 amino acids (aa 129–152 in SUZ12-L) that partially overlap with the WD-binding domain 1 (WDB1, 110–145). We reasoned that exon 4 skipping might alter the structure of SUZ12 and, possibly, PRC2 composition. To explore this possibility, we generated ESCs that lack the Suz12 exon 4 via CRISPR-Cas9–induced deletion. In addition, to rule out any biases due to the expression levels and/or SUZ12 epitope masking, we generated Suz12 knockout (KO) ESCs (herein, KO) in which Suz12 expression was subsequently rescued by re-introducing either the Suz12-L or Suz12-S mouse isoform fused to a triple-Flag tag under the regulation of a CAG promoter (KO+L/S; Figures S2H–S2K). We performed SUZ12 immunoprecipitation coupled with mass spectrometry (IP-MS) in the WT and ∆ex4 clones to compare their interactomes and with a flag antibody in the KO and rescue cell lines. As expected, no peptides corresponding to exon 4 were retrieved in ∆ex4 samples, while the rest of the sequence displayed similar coverage. Comparison of interactors in the two conditions revealed that SUZ12 binding to AEBP2 and JARID2 was strongly reduced in ∆ex4 cells with respect to WT cells, whereas SUZ12 binding to most core components or to PRC2.1-specific factors was unchanged or only slightly increased . These observations were confirmed by SUZ12 IP followed by Western blot (WB). Flag IP-MS in rescue cells confirmed that, while the long isoform was able to correctly form comparable amounts of both PRC2.1 and PRC2.2 subtypes, interaction of the SUZ12-S with PRC2.2-specific factors was drastically reduced.

2024-03-18 | PXD046660 | Pride

Change in H3K4me3 in Suz12(Bgal/Bgal) ESCs, and over Spinal Motor Neuron differentiation (ChIP-Seq)

Project description:Suz12(Bgal/Bgal) ESCs express a truncated form of Suz12 fused to Beta-galactosidase. These cells maintain a reduced level of H3K27me3 despite this mutation to a core component of PRC2, unlike Eed-/- ESCs whose H3K27me3 is ablated. This data shows the concomitant changes in H3K4me3 levels in these cells. An ESC line mutant in Suz12, a core component of Polycomb Repressive Complex 2, was assessed for H3K4me3 by ChIP-seq, as compared to a wild type ESC line, as well as both lines subjected to in vitro differentiation down the Spinal Motor Neuron pathway.

2014-11-17 | E-GEOD-61248 | biostudies-arrayexpress

Chromatin immunoprecipitation of human PolII and SUZ12 proteins in embryonic stem cells

Project description:Polycomb group proteins are essential for early development in metazoans but their contributions to human development are not yet well understood. We have mapped the Polycomb Repressive Complex 2 (PRC2) subunit Suz12 across the entire non-repeat portion of the genome in human embryonic stem (ES) cells. We found that Suz12 is distributed across large portions of over two hundred genes encoding key developmental regulators. These genes are occupied by nucleosomes trimethylated at histone H3K27, are transcriptionally repressed, and contain some of the most highly conserved non-coding elements in the vertebrate genome. We found that preferential activation of PRC2 target genes occurs during differentiation of ES cells into other cell types. The ES cell transcriptional regulators Oct4, Sox2 and Nanog co-occupied a significant subset of these genes, further supporting a link between repression of developmental regulators and stem cell pluripotency. These results indicate that PRC2 occupies a special set of developmental genes in ES cells that must be repressed to maintain pluripotency and that are poised for activation during ES cell differentiation.

2006-06-14 | E-WMIT-7 | biostudies-arrayexpress

Mapping early PRC2 nucleation sites upon Suz12 reintroduction reveals features of de novo Polycomb recruitment [RNA-seq]

Project description:Mapping early PRC2 nucleation sites upon Suz12 reintroduction reveals features of de novo Polycomb recruitment [RNA-seq]

| PRJNA1304347 | ENA