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Genome wide mapping of Jarid2 and Suz12 binding sites in mouse ES cells before and after Jarid2 depletion

ABSTRACT: We analyzed the overlap in genome wide binding sites between Jarid2 and Suz12 in mouse ES cells and find that Jarid2 and Suz12 peaks have an high degree (90%) of overlap. Moreover we analyzed the effect of Jarid2 down regulation on genome wide Suz12 binding sites and found that Loss of Jarid2 lead to the loss of 70% of Suz12 binding sites and to a 10 Fold reduction in intensity for 90% of Suz12 binding sites. Overall, these results demonstrate that Jarid2 plays an essential role for Suz12 (PRC2 complex) association to DNA.

ORGANISM(S): Mus musculus

PROVIDER: GSE19365 | GEO | 2010/01/27

SECONDARY ACCESSION(S): PRJNA120403

REPOSITORIES: GEO

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Genome wide mapping of Jarid2 and Suz12 binding sites in mouse ES cells before and after Jarid2 depletion

Project description:We analyzed the overlap in genome wide binding sites between Jarid2 and Suz12 in mouse ES cells and find that Jarid2 and Suz12 peaks have an high degree (90%) of overlap. Moreover we analyzed the effect of Jarid2 down regulation on genome wide Suz12 binding sites and found that Loss of Jarid2 lead to the loss of 70% of Suz12 binding sites and to a 10 Fold reduction in intensity for 90% of Suz12 binding sites. Overall, these results demonstrate that Jarid2 plays an essential role for Suz12 (PRC2 complex) association to DNA. Examination of two different proteins in two different cell lines

2010-01-27 | E-GEOD-19365 | 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

Jarid2, a Polycomb member and target of miR-155, regulates the fates of Th17 and Treg cells

Project description:Genome-wide analysis of Jarid2, Suz12, and c-Maf binding and H3K27me3 profiling in miR-155 KO and WT Th17 performed by ChIP-seq. We found that Jarid2 and c-Maf is differentially expressed in absence of miR-155 and they compete for binding to the Il22 promoter. We highlight targets of Jarid2 and Suz12 in miR-155 KO Th17 cells that are epigenetically silenced by increased H3K27me3 status. Furthermore, genome-wide analysis through Suz12 ChIP-exo in WT and Jarid2fl/fl;CD4cre Th17 reveals defects in PRC2 recruitment in abscence of Jarid2 that results in derepression of genes in Th17 cells. Thus, one main function of miR-155 is to curb epigenetic silencing by targeting Jarid2. Examination of Jarid2, Suz12, c-Maf binding and H3K27me3 changes in miR-155 KO and WT Th17.

2014-06-01 | E-GEOD-47528 | biostudies-arrayexpress

RNA-seq for ESC-derived CPs in presence or absence of SUZ12, MTF2, or JARID2

Project description:We performed mRNA-seq after differentiation of embryonic stem cells (ESCs) into cardiac precursors (CPs) with with or without inducing degradation of PRC2 subunits MTF2, JARID2, or SUZ12 using the AID system

2021-04-21 | GSE167043 | GEO

SUZ12 immunoprecipitation followed by PRM of SUZ12 peptides to identify alternatively spliced isoforms of SUZ12 at the protein level.

Project description:Alternative splicing of SUZ12 exon 4 is predicted to generate two alternative isoforms differing by the inclusion or exclusion of 69 nucleotides in exon 4, which we named SUZ12-long (SUZ12-L) and SUZ12-short (SUZ12-S) respectively. At the protein level 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). To detect the existance of SUZ12-S at the protein levels we performed SUZ12 immunoprecipitation coupled with mass spectrometry (IP-MS) in the WT and ∆ex4 clones to identify SUZ12-S unique peptides. We identified a SUZ12-S specific peptide in both WT #2 and ∆ex4 #1. These observations were confirmed by SUZ12 IP followed by Western blot (WB) (size shift).

2024-03-18 | PXD046742 | Pride

RNA-seq for ESC and NPC in presence or absence of SUZ12, MTF2, or JARID2

Project description:We performed mRNA-seq before and after differentiation of embryonic stem cells (ESCs) into neural progenitor cells (NPCs) with with or without inducing degradation of PRC2 subunits MTF2, JARID2, or SUZ12 using the AID system

2021-04-21 | GSE155990 | GEO

Jarid2, a Polycomb member and target of miR-155, regulates the fates of Th17 and Treg cells

2014-06-01 | GSE47528 | GEO

Jarid2/Jumonji coordinates control of PRC2 enzymatic activity and target gene occupancy in pluripotent cells

Project description:We report on mechanism of interaction between PRC2 complex and Jarid2 and their role in pluripotent cells Examination of PRC2 genomic localization by analysis of Jarid2, Ezh2, Suz12 and Jarid1a occupancy

2009-12-24 | E-GEOD-18776 | 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

Jarid2 regulates hematopoietic stem cell function by acting with Polycomb Repressive Complex 2

Project description:Polycomb Repressive Complex 2 (PRC2) has been shown to play a key role in hematopoietic stem and progenitor cell (HSPC) function. Analyses of mouse mutants harboring deletions of core components have implicated PRC2 in fine-tuning multiple pathways that instruct HSPC behavior, yet how PRC2 is targeted to specific genomic loci within HSPCs remains unknown. Here we use shRNA-mediated knockdown to survey the function of known PRC2 accessory factors in HSPCs by testing the competitive reconstitution capacity of transduced murine fetal liver cells. We find that similar to the phenotype observed upon depletion of core subunit Suz12, depleting Jarid2 enhances the competitive transplantation capacity of both fetal and adult, mouse and human HSPCs. Gene expression profiling revealed common Suz12 and Jarid2 target genes that are enriched for the H3K27me3 mark established by PRC2. These data implicate Jarid2 as an important component of PRC2 that has a central role in coordinating HSPC function. RNA-seq of jarid knockdown, suz knockdown and control from HSPC in 16 week old mice.

2015-04-02 | E-GEOD-60808 | biostudies-arrayexpress

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