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Histone H3 Trimethylation at Lysine 36 (H3K36me3) Guides m6A RNA Modification

ABSTRACT: Histone H3 Trimethylation at Lysine 36 (H3K36me3) Guides m6A RNA Modification

PROVIDER: PRJNA433476 | ENA |

REPOSITORIES: ENA

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Histone H3 Trimethylation at Lysine 36 (H3K36me3) Guides m6A RNA Modification

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

2019-02-21 | GSE110323 | GEO

SMYD5 catalyzes histone H3 lysine 36 trimethylation at promoters

Project description:SMYD5 catalyzes histone H3 lysine 36 trimethylation at promoters

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SMYD5 catalyzes histone H3 lysine 36 trimethylation at promoters

Project description:Histone mark, one carrier of epigenetic information, regulates the gene expression in cells. Studies have shown that H3K36me3 is mainly catalyzed by SETD2 to be deposited at gene body regions in mammalian cells. Here, we profile the distributions of H3K36me3 in native cells and uncover that H3K36me3 is also enriched at the promoters beyond the gene body regions. We identify SMYD5 as one methyltransferase responsible for the enrichment of H3K36me3 at promoters. Through RNA polymerase II, SMYD5 is recruited to chromatin to regulate H3K36me3 and gene expression. The enzymatic activity of SMYD5 is dependent on its C-terminal glutamic acid rich domain. Depletion of C-terminal domain reduces the reestablishment of H3K36me3 at promoters when Smyd5 is over-expressed in Smyd5 knockout cells. Furthermore, elevated Smyd5 expression contributes to the tumorigenesis of liver hepatocellular carcinoma. Together, our study reveals SMYD5 as the H3K36me3 methyltransferase at promoters to regulate the gene expression, providing important insights into the localization and function of H3K36me3.

2022-04-26 | GSE184894 | GEO

Profiling of Histone H3 Trimethylation at Lysine 36 (H3K36me3) in HepG2 cells: SETD2 knockdown and control cells

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

Profiling of Histone H3 Trimethylation at Lysine 36 (H3K36me3) in HepG2 cells: SETD2 knockdown and control cells

Project description:Profiling of Histone H3 Trimethylation at Lysine 36 (H3K36me3) in HepG2 cells: SETD2 knockdown and control cells

| PRJNA433473 | ENA

Histone H3 trimethylation at lysine 36 guides m<sup>6</sup>A RNA modification co-transcriptionally.

Project description: Not available

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CHD8 Suppression Impacts on Histone H3 Lysine 36 Trimethylation and Alters RNA Alternative Splicing

Project description:Disruptive mutations in the chromodomain helicase DNA binding protein 8 (CHD8) have been recurrently associated with Autism Spectrum Disorders (ASD). Here we investigated how chromatin reacts to CHD8 suppression by analyzing a panel of histone modifications in induced pluripotent stem cell-derived neural progenitors. CHD8 suppression led to significant reduction (47.82%) in histone H3K36me3 peaks at gene bodies, particularly impacting on transcriptional elongation chromatin states. H3K36me3 reduction specifically affects highly expressed, CHD8-bound genes and correlates with altered alternative splicing patterns of 408 genes implicated in “regulation of RNA splicing”, “mRNA catabolic process”. Interestingly, mass-spectrometry analysis uncovered a novel interaction between CHD8 and the splicing regulator Heterogeneous Nuclear Ribonucleoprotein L (hnRNPL), providing the first mechanistic insights to explain CHD8-suppression splicing phenotype, partially implicating SETD2, H3K36me3 methyltransferase. In summary, our results point toward broad molecular consequences of CHD8 suppression, entailing altered histone deposition/maintenance and RNA processing regulation as important regulatory processes in ASD.

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Profiling of Histone H3 Trimethylation at Lysine 36 (H3K36me3) in mouse embryonic stem cells: Setd2 knockdown and control cells

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

Profiling of Histone H3 Trimethylation at Lysine 36 (H3K36me3) in mouse embryonic stem cells: Setd2 knockdown and control cells

Project description:Profiling of Histone H3 Trimethylation at Lysine 36 (H3K36me3) in mouse embryonic stem cells: Setd2 knockdown and control cells

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Trimethylation of histone H3 lysine 36 by human methyltransferase PRDM9 protein.

Project description: Not available

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