Role of Setd2 in regulatory T cells [H3K36me3 ChIP-seq]
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA755957 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR15509618.fastq.gz | Fastqsanger.gz | |||
| SRR15509619.fastq.gz | Fastqsanger.gz | |||
| SRR15509620.fastq.gz | Fastqsanger.gz |
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Project description:ChIP-sequencing for H3K36me3 analysis was performed on Tregs purified from the spleen and large intestine of naïve mice.
2022-10-14 | GSE182340 | GEO
Project description:SETD2 is the specific methyltransferase of H3K36me3. To obtain SETD2-dependent landscape of H3K36me3 in human genome, we performed ChIP sequencing in SETD2 silenced and control HepG2 cells.
2019-02-21 | GSE110318 | GEO
Project description:Histone-Lysine N-methyltransferase SETD2 is an evolutionarily conserved histone methyltransferase that associates with RNA Polymerase II (RNAPII) and catalyzes trimethylation of histone H3 lysine 36 (H3K36me3) in transcribed regions. Interestingly, SETD2 is frequently mutated in cancers. Clear cell renal cell carcinomas (ccRCCs) have extensive mutation of SETD2, implicating SETD2 as a tumor suppressor. ccRCCs are known for early driving events where the 3p chromosomal arm is lost, deleting one copy of SETD2, resulting in haploinsufficiency. While the role of SETD2 mediated H3K36me3 and interaction of RNAPII has been the focus of many studies, haploinsufficient SETD2 tumors retain H3K36me3, yet have drastic genome stability defects. The C-terminus of SETD2 is required for H3K36me3 while the N-terminus of SETD2 remains poorly characterized compared to the C-terminus. The N-terminus is highly disordered and has recently been shown to contribute to SETD2 stability, implicating regulatory functions. To better understand how SETD2 contributes to chromatin biology, we first sought to identify SETD2 protein interactors. A stable, immortalized normal human kidney epithelial cell (HKC) line with a dox inducible SETD2-APEX2 construct was used for a proximity-based biotinylation assay. Initial analysis yielded 2083 biotinylated proteins with significant enrichment (log2 fold change > 2 p-value < 0.05) in SETD2-APEX2 compared to control. Gene Ontology analysis of these interactors revealed enrichment of proteins involved in nuclear envelope functions, including lamin A/C, lamin B1, lamin B2 and emerin. These interactions were confirmed via western and reciprocal immunoprecipitation (IP). To determine effect of SETD2 depletion on lamin A/C and lamin B1 phosphorylation, we performed lamin A/C or lamin B1 IP from control or SETD2-knockdown (KD) cells and interrogated via LC-MS/MS. Mass spectrometry analysis revealed a significant decrease in lamin A/C S22 phosphorylation, and modest decrease in S390 phosphorylation, in SETD2 depleted cells compared to controls. While lamin B1 S23 phosphorylation was detected in control cells, we did not detect it in SETD2-KD cells, indicating a significant reduction in S23 phosphorylation upon SETD2 depletion. Next, we sought to identify the effect of SETD2 N-terminal deletion on the SETD2 protein interactome. We compared the protein interactors of dox inducible WT-SETD2 APEX2 fusion to an N-terminal deletion mutant of SETD2 (tSETD2-APEX2). Deletion of the N-terminus resulted in loss of lamin B1 and emerin interaction. Intriguingly, tSETD2 selectively associated with lamin C, whereas WT SETD2 interacted with both lamin A and C. These data together reveal an interaction with SETD2 and nuclear lamins. Further experiments revealed a role for the SETD2 N-terminus in facilitating the association of lamins with CDK1, thereby promoting lamin phosphorylation and depolymerization required for nuclear envelope disassembly during mitosis. Together, the data reveal a non-catalytic role of SETD2 during mitosis.
2025-06-04 | PXD040771 | Pride
Project description:Role of Setd2 in regulatory T cells
| PRJNA758052 | ENA
Project description:Spermatogenesis is precisely cotrolled by complex gene expression programs and involves epigenetic reprogramming including histone modification and DNA methylation. Setd2 catalyzes the trimethylation of histone H3 Lys36 (H3K36me3) and plays key roles in embryonic stem cell differentiation and somatic cell development; however, its role in male germ cell development remains elusive. Here we demonstrate an essential role of Setd2 for spermiogenesis. We show that targeted knockout of Setd2 in germ cells causes aberrant spermiogenesis with acrosomal malformation before step 8 round spermatid stage, resulting in complete male infertile. Furthermore, we show a complete loss of H3K36me3 and a significant altered gene expression profile, including Acrbp1 and protamines, caused by Setd2 deficiency. Our findings reveal a previously underappreciated role of Setd2-dependent H3K36me3 for spermiogenesis and improved the understanding of epigenetic disorders underlying male infertility.
2018-04-28 | GSE108717 | GEO
Project description:Setd2 is the specific methyltransferase of H3K36me3. To obtain Setd2-dependent landscape of H3K36me3 in mouse genome, we used mouse embryonic stem cells (mESCs) model with doxycycline (Dox)-induced Setd2 knockdown, and performed ChIP sequencing in mESCs with or without Dox treatment.
2019-02-21 | GSE110321 | GEO
Project description:We performed RNA-seq of 293T cells post depletion and SETD2 or hnRNP L to compare their global transcriptome profile. We also looked at the distribution of the histone mark H3K36me3 in wild type 293T to correlate it with the observed transcriptome changes upon SETD2 and hnRNP L depletion. We rescued SETD2 knock out 293T cells with SETD2 FL (Full Length), FLΔSRI (FLwoSRI) and FLΔSHI (FLwoSHI) and performed H3K36me3 ChIP-Seq.
2021-01-29 | GSE151296 | GEO
Project description:Purpose: The goal of this study is to identify differential Setd2-mediated H3K36me3 modificaion in the resolution phase of inflammation induced by LPS Methods: We profiled chip-seq with H3K36me3 antibody in bone marrow-derived macrophages stimulated with LPS for 0h, 4h, 16h. Results: We find different H3K36me3 enrichment peaks under LPS stimulation at different time.
2024-11-13 | GSE141470 | GEO
Project description:During the aging process, bone marrow mesenchymal stem cells (BMSCs) exhibit declined osteogenesis accompanied by excess adipogenesis, which will lead to osteoporosis. Here we report that the H3K36 trimethylation, catalyzed by histone methyltransferase SETD2 regulates lineage commitment of BMSCs. Deletion of Setd2 in mBMSCs, through conditional Cre expression driven by Prx1 promoter, resulted in bone loss and marrow adiposity. Loss of Setd2 in BMSCs in vitro facilitated differentiation propensity to adipocytes rather than to osteoblasts. Through conjoint analysis of RNA-seq and ChIP-seq data, we identified a SETD2 functional target gene, Lbp, on which H3K36me3 was enriched, and its expression was affected by Setd2 deficiency. Furthermore, overexpression of LBP could partially rescue the lack of osteogenesis and enhanced adipogenesis resulted from the absence of Setd2 in BMSCs. Further mechanism study demonstrated that the trimethylation level of H3K36 could regulate Lbp transcriptional initiation and elongation. These findings suggest that H3K36 trimethylation mediated by SETD2 could regulate the cell fate of mesenchymal stem cells in vitro and in vivo, indicating that the regulation of H3K36me3 level by targeting SETD2 and/or the administration of downstream LBP protein may represent potential therapeutic way for new treatment in metabolic bone diseases, such as osteoporosis.
2018-11-08 | GSE120351 | GEO
Project description:Role of Setd2 in regulatory T cells [RNAseqTreg]
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