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ScRNA-seq of EZH2-knockout Memory B cells

ABSTRACT: To understand the transcriptional circuits controled by the histone methyltransferase EZH2 in memory B cells (MBC) scRNA-seq was performed on influenza-specific MBC that formed at an early day 14 or late day 39 time point. EZH2-knockout MBC were compared to CRE control MBC isolated from the spleens and mediastinal lymph nodes of mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE274127 | GEO | 2025/01/02

REPOSITORIES: GEO

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EZH2 is required for gene repression in Plasmablasts

Project description:To understand the role of EZH2 in Plasmablast function EZH2 was inducibly deleted using tamoxifen and B cells stimulated to differentiate with LPS in vivo. After 3 days, CD138+ cells were enriched from the spleens and RNA-seq was performed to identify the genes targeted by EZH2 for repression.

2017-12-16 | GSE103126 | GEO

EZH2-dependent chromatin accessibility changes during B cell differentiation

Project description:To understand the role of EZH2 in B cell differentiation, EZH2 was inducibly deleted using tamoxifen and B cells stimulated to differentiate with LPS in vivo. After 3 days, EZH2-sufficient and EZH2-deficient naive B cells and plasmablasts were FACS isolated from the spleens and ATAC-seq was performed to identify the chromatin accessibility changes that are programmed by EZH2.

2017-12-16 | GSE103142 | GEO

Affinify Purification of EZH2 and phosphodeficient EZH2 identifies phosphorylation dependent interactions of EZH2

Project description:Overexpression of EZH2 in estrogen receptor negative (ER-) breast cancer promotes metastasis. EZH2 has been mainly studied as the catalytic component of the Polycomb Repressive Complex 2 (PRC2) that mediates gene repression by trimethylating histone H3 at lysine 27 (H3K27me3). However, how EZH2 drives metastasis despite the low H3K27me3 levels observed in ER- breast cancer is unknown. We have shown that in human invasive carcinomas and distant metastases, cytoplasmic EZH2 phosphorylated at T367 is significantly associated with ER- disease and low H3K27me3 levels. Here, we explore the interactome of EZH2 and of a phosphodeficient mutant EZH2_T367A. We identified novel interactors of EZH2, and identified interactions that are dependent on the phosphorylation and cellular localization of EZH2 that may play a role in EZH2 dependent metastatic progression.

2018-07-03 | PXD010073 | Pride

Transcriptomic profile of recovered exogenous Tregs from injured bone, muscle, and skin of mice that were locally treated with Tregs, as well as heart, MLN and spleen from mice with MI that were systemically treated with Tregs.

Project description:Transcriptomic profile of recovered exogenous Tregs from injured bone, muscle, and skin of mice that were locally treated with Tregs, as well as heart, mediastinal lymph nodes (MLN) and spleen from mice with myocardial infarcts (MI) that were systemically treated with Tregs. Mice with tissue injuries were treated with exogenous Tregs that were sorted from spleens of Foxp3(IRES-mRFP) mice - C57BL6/J mice with bone, muscle and skin injuries were treated via hydrogel-mediated local delivery of Tregs soon after injury, while mice with myocardial infarcts (MI) were treated with systemic (intravenous) delivery of Tregs one day post-MI. Three days after Treg-delivery, the injured bone, muscle, and skin tissues, as well as heart, mediastinal lymph nodes and spleens from mice with MI were harvested, and the exogenous (delivered) Tregs were recovered by FACS sorting. These sorted exogenous Tregs recovered at day 3 post-Treg delivery (Day 3 recovered Tregs) were then used for mini-bulk RNA sequencing along with spleen Tregs before delivery as a control (Day 0 Spleen Tregs).

2024-05-31 | GSE230177 | GEO

EZH2-mediated H3K27me3 targets transcriptional circuits of neuronal differentiation

Project description:EZH2-mediated H3K27me3 targets transcriptional circuits of neuronal differentiation

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Role of Ezh2 on Skeletal Development

Project description:To study the role of Ezh2 in growth plate, we generated Ezh1 complete knockout, Ezh2 cartilage-specific knockout mice (Ezh1-/-, Col2-cre Ezh2 f/f) and compared it with Ezh2 wildtype littermates (Ezh1 -/-, Col2-cre Ezh2 +/+). Proliferative zone (PZ) and Hypertrophic zones (HZ) of proximal tibial growth plate were dissected from 3-day old mice by laser capture microdissection and RNA were isolated by pico pure RNA isolation kit

2016-11-09 | GSE84198 | GEO

The regulatory roles of Ezh2 in response to lipopolysaccharide (LPS) in macrophages and mice with conditional Ezh2 deletion with LysM-Cre system

Project description:The responses of macrophages to lipopolysaccharide (LPS) might determine the direction of clinical manifestations of sepsis, which is the immune response against severe infection. Meanwhile, the enhancer of zeste homologue 2 (Ezh2), a histone lysine methyltransferase of epigenetic regulation, might interfere with LPS response. With a single LPS stimulation, Ezh2 null(Ezh2flox/flox; LysM-Crecre/−) macrophages demonstrated lower supernatant TNF-α than Ezh2 control (Ezh2fl/fl; LysM-Cre−/−), perhaps due to an upregulation of Socs3, which is a suppressor of cytokine signaling 3, due to the loss of the Ezh2 gene. In LPS tolerance, Ezh2 null macrophages indicated higher supernatant TNF-α and IL-6 than the control, supporting an impact of the loss of the Ezh2 inhibitory gene. In parallel, Ezh2 null mice demonstrated lower serum TNF-α and IL-6 than the control mice after an LPS injection, indicating a less severe LPS-induced hyper-inflammation in Ezh2 null mice. In conclusion, an absence of Ezh2 in macrophages resulted in less severe LPS-induced inflammation, as indicated by low serum cytokines, with less severe LPS tolerance, as demonstrated by higher cytokine production, partly through the upregulated Socs3.

2023-07-20 | PXD041265 | Pride

Bottom-up proteomics of EZH2 mutants in isogenic cells

Project description:The Enhancer of Zeste 2 Polycomb Repressive Complex 2 Subunit (EZH2) is an essential epigenetic modifier able to methylate lysine 27 on histone H3 (H3K27) to induce chromatin compaction, protein complex recruitment and ultimately transcriptional repression. Hematologic malignancies, including Diffuse Large B cell lymphoma (DLBCL) and Acute myeloid leukemia (AML) have shown a high EZH2-mutation frequency (>20%) associated with poor clinical outcomes. Particularly, two distinct oncogenic mutations, so-called gain-of-function (Y641F and A677G) and loss-of-function (H689A and F667I) are found in the catalytic domain of EZH2. In this study, a comprehensive multi-omics approach was employed to characterize downstream effects of H3K27me3 deposition driven by EZH2 mutations. Human embryonic kidney cells (HEK293T) were transfected to generate three stable EZH2 mutants: EZH2(Y641F), EZH2(A677G), and EZH2(H689A/F667I), which were validated via immunoblotting and DIA-MS-based histone profiling assay. Subsequently, constructs were analyzed under a comprehensive multi-omics approach including label-free whole-cell proteomics, acquired with a Bruker timsTOF Pro HPLC-MS/MS with Ion Mobility. Important protein interactors at nuclear level were dysregulated, such as SMYD3 (SET and MYND domain containing 3), NSD2 (nuclear receptor binding SET domain protein 2) and CHD7 (chromodomain helicase DNA binding protein 7), suggesting a cooperative network of chromatin remodelers for gene expression reprogramming.

2023-10-24 | PXD042875 | Pride

Histone PTM profiling analysis of EZH2 mutants in isogenic cells

Project description:The Enhancer of Zeste 2 Polycomb Repressive Complex 2 Subunit (EZH2) is an essential epigenetic modifier able to methylate lysine 27 on histone H3 (H3K27) to induce chromatin compaction, protein complex recruitment and ultimately transcriptional repression. Hematologic malignancies, including Diffuse Large B cell lymphoma (DLBCL) and Acute myeloid leukemia (AML) have shown a high EZH2-mutation frequency (>20%) associated with poor clinical outcomes. Particularly, two distinct oncogenic mutations, so-called gain-of-function (Y641F and A677G) and loss-of-function (H689A and F667I) are found in the catalytic domain of EZH2. In this study, a comprehensive multi-omics approach was employed to characterize downstream effects of H3K27me3 deposition driven by EZH2 mutations. Human embryonic kidney cells (HEK293T) were transfected to generate three stable EZH2 mutants: EZH2(Y641F), EZH2(A677G), and EZH2(H689A/F667I), which were validated via immunoblotting and DIA-MS-based histone profiling assay. The histone profiling assay demonstrated a significant increase of approximately two-fold in H3.1/H3.3K27me3 for Y641F EZH2 mutant. There was a modest increase in the combinatorial PTMs H3.1/H3.3K27me3K36me1 and a significant depletion in H3.1 and H3.3 K27me2. The most depleted peptide was H3.3K27me2K36me2. For the A677G EZH2 mutant, the assay demonstrated an enrichment on H3.1/H3.3K27me3, combinatorial K27me3K36me1 and a slight increase in K27me1 and K18ac but only on H3.1. The most depleted peptide was H3.3K27me2K36me2. The H689A/F667I cell line has the most alterations in global histone PTMs. The most highly enriched were H3.1/H3.3K36me2, H3.1K9me3 and H3.3K36me1. The most depleted modifications were H3.1K23ac and H3.1K27me3.

2023-10-24 | PXD042953 | Pride

Early NKT cell wave of IL-4 serves as an innate link to support initiation of B cell immunity during infection

Project description:IL-4/GFP- enhanced transcript (4Get) reporter mice were infected with 200 PFU of Influenza A virus PR8 strain. At day 3 of infection, mediastinal lymph nodes were harvested and GFP+ cells sorted and separated by their ability to bind a CD1d-tetramer (Tet+ n=133 , Tet- n=109 ). Single-cell RNA-Seq was used to identify subpopulations of IL-4 producing cells. Single-cell transcriptomes were clustered using Seurat and differentially expressed genes within each cluster were used to resolve IL-4+ subpopulations and aid in defining their role in initiating B cell immunity during influenza infection.

2017-12-14 | GSE103753 | GEO

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