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Impact of heterozygous SRI mutation (R2483H) of Setd2 (Setd2SRI/wt) on H3K36me3 patterns in the brains of mouse neonates

ABSTRACT: We report that only a limited genes have differential H3K36me3 marks in the brains of heterozygous Setd2SRI/wt mice compared to those of wild type mice at P0.

ORGANISM(S): Mus musculus

PROVIDER: GSE173092 | GEO | 2021/09/08

REPOSITORIES: GEO

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Impact of heterozygous SRI mutation (R2483H) of Setd2 (Setd2SRI/wt) on gene expression in the brains of mouse neonates

Project description:We report that only a limited number of genes are differentially expressed in the brains of heterozygous Setd2SRI/wt mice compared to those of wild type mice at P0.

2021-09-08 | GSE173090 | GEO

Impact of heterozygous SRI mutation (R2483H) of Setd2 (Setd2SRI/wt) on H3K36me3 patterns in the brains of mouse neonates

Project description:Impact of heterozygous SRI mutation (R2483H) of Setd2 (Setd2SRI/wt) on H3K36me3 patterns in the brains of mouse neonates

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Impact of heterozygous SRI mutation (R2483H) of Setd2 (Setd2SRI/wt)

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-09-08 | GSE173093 | GEO

Impact of heterozygous SRI mutation (R2483H) of Setd2 (Setd2SRI/wt) on gene expression in the brains of mouse neonates

Project description:Impact of heterozygous SRI mutation (R2483H) of Setd2 (Setd2SRI/wt) on gene expression in the brains of mouse neonates

| PRJNA723811 | ENA

Impact of heterozygous SRI mutation (R2483H) of Setd2 (Setd2SRI/wt)

Project description:Impact of heterozygous SRI mutation (R2483H) of Setd2 (Setd2SRI/wt)

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Setd2 reprograns lipid metabolism for the resolution of inflammation via H3K36me3 modification

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

Role of Setd2 in regulatory T cells [H3K36me3 ChIP-seq]

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

SPOP-containing complex regulates SETD2 stability and H3K36me3-coupled alternative splicing.

Project description:Trimethylation of histone H3K36 is a chromatin mark associated with active gene expression, which has been implicated in coupling transcription with mRNA splicing and DNA damage response. SETD2 is a major H3K36 trimethyltransferase, which has been implicated as a tumor suppressor in mammals. Here, we report the regulation of SETD2 protein stability by the proteasome system, and the identification of SPOP, a key subunit of the CUL3 ubiquitin E3 ligase complex, as a SETD2-interacting protein. We demonstrate that SPOP is critically involved in SETD2 stability control and that the SPOP/CUL3 complex is responsible for SETD2 polyubiquitination both in vivo and in vitro ChIP-Seq analysis and biochemical experiments demonstrate that modulation of SPOP expression confers differential H3K36me3 on SETD2 target genes, and induce H3K36me3-coupled alternative splicing events. Together, these findings establish a functional connection between oncogenic SPOP and tumor suppressive SETD2 in the dynamic regulation of gene expression on chromatin.

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SETD2-mediated crosstalk between H3K36me3 and H3K79me2 in MLL-rearranged leukemia.

Project description:Previously, we identified SETD2 loss-of-function mutations in 22% of MLL-rearranged (MLLr) acute leukemia patients, implicating a mechanism for cooperativity between SETD2 mutations and MLL fusions. However, the detailed mechanism of how SETD2-H3K36me3 downregulation accelerates MLLr leukemia remains unclear. Here, we show that in MLLr leukemia, both H3K79me2 and H3K36me3 are aberrantly elevated and co-enriched in a group of genes. SETD2 inactivation leads to a global reduction of H3K36me3 and a further elevation of H3K79me2, but does not change the expression of known MLL fusion target genes. Instead, this pattern of histone changes is associated with transcriptional deregulation of a novel set of genes; downregulating tumor suppressors (for example, ASXL1) and upregulating oncogenes (for example, ERG). Taken together, our findings reveal a global crosstalk between the oncogenic DOT1L-H3K79me2 axis and the tumor suppressive SETD2-H3K36me3 axis in gene regulation, provide molecular insights into how SETD2 mutations accelerate MLLr leukemogenesis through differential regulation of additional tumor suppressors and oncogenes.

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Targeted Profiling of Epitranscriptomic Reader, Writer and Eraser Proteins Regulated by H3K36me3

Project description:Trimethylation of lysine 36 on histone H3 (H3K36me3), an epigenetic mark associated with actively transcribed genes, plays an important role in multiple cellular processes, including transcription elongation, DNA methylation, DNA repair, and RNA m6A methylation, etc. Aberrant expression and mutations of the main methyltransferase for H3K36me3, i.e., SET domain-containing 2 (SETD2), were shown to be associated with various cancers. Here, we performed targeted profiling of 154 epitranscriptomic RWE proteins using a scheduled liquid chromatography-parallel-reaction monitoring (LC-PRM) method coupled with the use of stable isotope-labeled (SIL) peptides as internal standards to investigate how H3K36me3 modulates the chromatin occupancies of epitranscriptomic reader, writer, and eraser (RWE) proteins. Our results showed consistent changes in chromatin occupancies of RWE proteins upon losses of H3K36me3 and H4K16ac, and a role of H3K36me3 in recruiting METTL3 to chromatin upon DNA double strand break induction. In addition, protein-protein interaction network and Kaplan-Meier survival analyses revealed the importance of METTL14 and TRMT11 in kidney cancer. Taken together, our work revealed cross-talks between H3K36me3 and epitranscriptomic RWE proteins and uncovered potential roles of these RWE proteins in H3K36me3-mediated biological processes.

2023-05-25 | PXD041343 | Pride

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