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H3K36me3 and H3K27me3 occupancy profiling by high throughput sequencing from setd2 wt and ko germinal center B cells and H3K27me3 occupancy profiling by high throughput sequencing from phf19 wt and ko germinal center B cells

ABSTRACT: Our study aims to understand the H3K36me3 and H3K27me3 genome-wide alterations by analysing CHIP-seq data between setd2 wt and ko germinal center B cells, characterize the function of H3K36me3 methyltransferase setd2 in H3K36me3 itself and H3K27me3, further we aim to H3K27me3 from phf19 ,which is H3K27me3 regulator, WT and KO group to investigate the mechanism of H3K36me3 dependent H3K27me3 modification introduced by setd2.

ORGANISM(S): Mus musculus

PROVIDER: GSE184043 | GEO | 2024/09/14

REPOSITORIES: GEO

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H3K36me3 and H3K27me3 occupancy profiling by high throughput sequencing from setd2 wt and ko germinal center B cells and H3K27me3 occupancy profiling by high throughput sequencing from phf19 wt and ko germinal center B cells

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SETD2 haploinsufficiency enhances germinal center-associated AICDA somatic hypermutation to drive B-cell lymphomagenesis

Project description:SETD2 is the sole chromatin modifier responsible for H3K36me3, a histone mark linked to splicing, transcription initiation and DNA damage response. Homozygous disruption of SETD2 yields a tumor suppressor effect in various cancers. However, SETD2 mutation is virtually always heterozygous in diffuse large B-cell lymphomas (DLBCL). Here we show that heterozygous SETD2 deficiency results in germinal center (GC) hyperplasia and accelerated lymphomagenesis. SETD2 haploinsufficient GC B-cells exhibit increased competitive fitness and reduced DNA damage checkpoint activity, resulting in decreased apoptosis. SETD2 haploinsufficient GCB and lymphoma cells featured increased off- and on-target AICDA induced somatic hypermutation (SHM), complex structural variants such as rygma, and increased translocations including those activating MYC. DNA damage was selectively increased on the non-template strand and H3K36me3 loss was associated with greater RNA Pol II processivity and mutational burden, suggesting that SETD2-mediated H3K36me3 is required for proper sensing of cytosine deamination during transcription. Hence, SETD2 haploinsufficiency delineates a novel GC B-cell context specific oncogenic pathway involving defective epigenetic surveillance of AICDA mediated somatic hypermutation induced off target effects on transcribed genes.

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CUT&Tag sequencing in PDAC cells with Setd2-KO and Setd2-WT sorted from orthotopic PDAC tumor

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H3K36me2 occupancy profiling by high throughput sequencing from nsd2 wt and ko germinal center B cells

Project description:WHSC1 catalyzes dimethylation of lysine 36 on histone H3, which is upregualted in germinal center B cells. This study aimed to understand the H3K36me2 genome-wide alterations by analysing CHIP-seq data between wt and ko germinal center B cells.

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Expression data and H3K27me3 occupancy profiling by high throughput sequencing from control and SETD2 knockout organoids cells.

Project description:To understand the molecular basis how Setd2 loss enhances metastatic traits of PCa, we carried out RNA-seq and H3k27me3 Chip-seq using mice-derived prostatic organoid cells from 3-month-old PtenPC+/− and PtenPC+/−;Setd2PC−/− mice.To further validate Setd2 loss accelerated prostate tumorigenesis is dependent on EZH2 upregulation,we conduct high throughput sequencing of organoid cells derived from PtenPC+/− and PtenPC+/−;Setd2PC−/− mice with Ezh2 knockout.To understand the molecular basis whether the tumor suppressive function of Setd2 is depends on its methylation of EZH2 at k735, we also carried out RNA-seq using mice-derived prostatic organoid cells from 2-month-old PtenPC-/- and PtenPC-/-;Ezh2K735R mice.We integrated all the RNA-seq and chip-seq data generated from organoid cells.

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CUT&Tag analysis of H3K36me3 and H3K27me3, in Setd2-WT and -KO murine PDAC cell line

Project description:CUT&Tag analysis of H3K36me3 and H3K27me3, in Setd2-WT and -KO murine PDAC cell line

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H3K36me3 occupancy profiling by high throughput sequencing from control(APCmin) and APCmin; Setd2IEC-/- mice intestinal cells [ChIP-seq]

Project description:Setd2 catalyzes trimethylation of lysine 36 on histone H3. We conduct ChIP sequencing in chromatin landscape induced by Setd2 depleted in mouse intestinal cells to understand the H3K36me3 genome-wide alterations.

2017-09-01 | GSE95662 | GEO

Setd2 overexpression rescues bivalent gene expression during SCNT-mediated ZGA by enhancing H3K36me3 at gene bodies and excluding H3K27me3 from promoters [ChIP-seq]

Project description:Successful cloning through somatic cell nuclear transfer (SCNT) face significant challenges due to epigenetic obstacles. Recent studies have highlighted the roles of H3K4me3 and H3K27me3 as potential epigenetic barriers. However, the underlying mechanisms remain largely unclear. In this study, we generated genome-wide maps of H3K4me3 and H3K27me3 from mouse pre-implantation NT embryos. Our analysis revealed aberrant over-representation of H3K4me3 and H3K27me3 bivalent in 2-cell stage NT embryos, potentially linked to the deficiency of H3K36me3. Notably, the overexpression of Setd2, a H3K36me3 methyltransferase, successfully restored multiple epigenetic marks, including H3K36me3, H3K4me3 and H3K27me3. Additionally, it reinstated the expression levels of ZGA-related genes by re-establishing H3K36me3 at gene body regions to exclude H3K27me3 from bivalent regions, and ultimately improved cloning efficiency. These findings highlight the excessive bivalent state as a potent barrier and emphasize the removal of these barriers as a promising approach to achieving higher cloning efficiency.

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