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H3K27me3 Cut&Tag profiling of bone marrow-derived alveolar macrophages from wildtype and Suz12 knockout mice

ABSTRACT: Macrophages are at the forefront of immune responses and their transcriptional programs are modified by their tissue environment and in response to immunological challenge. Post-translational modifications of histones, such as histone H3 lysine 27 tri-methylation (H3K27me3) by the polycomb repressive complex 2 (PRC2), are tightly associated with epigenetic regulation of gene expression. To explore whether H3K27me3 is involved in either the establishment or function of the mononuclear phagocyte system, we selectively deleted the SUZ12 gene in mice, a core component of PRC2. Consistent with the the role of PRC2 in maintaining transcriptional repression, we found that the majority of top-ranked genes enriched for H3K27me3 in wild type alveolar macrophages were upregulated in SUZ12 knock-out alveolar macrophages.

ORGANISM(S): Mus musculus

PROVIDER: GSE176148 | GEO | 2021/12/22

REPOSITORIES: GEO

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RNA-seq profiling of foetal-derived alveolar macrophages from wildtype and Suz12 knockout mice

Project description:Macrophages are at the forefront of immune responses, and their transcriptional programs are modified by their tissue environment and in response to immunological challenge. Post-translational modifications of histones, such as histone H3 lysine 27 tri-methylation (H3K27me3) by the polycomb repressive complex 2 (PRC2), are tightly associated with epigenetic regulation of gene expression. To explore whether H3K27me3 is involved in either the establishment or function of the mononuclear phagocyte system, we selectively deleted the SUZ12 gene in one-week old mice, a core component of PRC2. SUZ12 ablation induced a rapid loss of the alveolar macrophage networks under both steady state and inflammatory conditions. Ablation of SUZ12 abrogated the proliferation of these cells required for their self-renewal.

2021-12-22 | GSE176115 | GEO

RNA-seq profiling of bone marrow-derived alveolar macrophages from wildtype and Suz12 knockout mice

Project description:Macrophages are at the forefront of immune responses and their transcriptional programs are modified by their tissue environment and in response to immunological challenge. Post-translational modifications of histones, such as histone H3 lysine 27 tri-methylation (H3K27me3) by the polycomb repressive complex 2 (PRC2), are tightly associated with epigenetic regulation of gene expression. To explore whether H3K27me3 is involved in either the establishment or function of the mononuclear phagocyte system, we selectively deleted the SUZ12 gene in mice, a core component of PRC2. SUZ12 ablation induced a rapid loss of the alveolar macrophage networks under both steady state and inflammatory conditions. Ablation of SUZ12 abrogated the proliferation of these cells required for their self-renewal.

2021-12-22 | GSE176111 | GEO

RNA-seq profiling of bone marrow-derived alveolar macrophages, foetal-derived alveolar macrophages and foetal-derived Langerhans cells from the lungs of wildtype and Suz12 knockout mice

2021-12-22 | GSE176117 | GEO

RNA-seq profiling of foetal-derived Langerhans cells from wildtype and Suz12 knockout mice

2021-12-22 | GSE176116 | GEO

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 [RNA-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. RNA-seq was performed in wild type and Suz12(Bgal/Bgal) ESCs, here used to demonstrate the coverage of the Suz12 gene in mRNA reads.

2013-07-22 | E-GEOD-47484 | biostudies-arrayexpress

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

2013-07-22 | GSE47484 | GEO

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

2013-07-22 | GSE47483 | 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.

2013-07-22 | E-GEOD-47483 | 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

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