Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

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

PROVIDER: PRJNA622964 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR11477100.fastq.gz	Fastqsanger.gz
	SRR11477101.fastq.gz	Fastqsanger.gz
	SRR11477102.fastq.gz	Fastqsanger.gz
	SRR11477103.fastq.gz	Fastqsanger.gz
	SRR11477104.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 51

Similar Datasets

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.

2023-03-11 | PXD025739 | Pride

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 462 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.

2022-01-31 | GSE148057 | GEO

SMYD5 catalyzes histone H3 lysine 36 trimethylation at promoters

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

| PRJNA766856 | ENA

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 gene (CHD8) have been recurrently associated with autism spectrum disorders (ASDs). 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 462 genes implicated in 'regulation of RNA splicing' and 'mRNA catabolic process'. 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 the CHD8 suppression-derived splicing phenotype, partly implicating SETD2, a 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.

| S-EPMC9825192 | biostudies-literature

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

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

| PRJNA433476 | ENA

SMYD5 catalyzes histone H3 lysine 36 trimethylation at promoters.

Project description:Histone marks, carriers of epigenetic information, regulate gene expression. In mammalian cells, H3K36me3 is mainly catalyzed by SETD2 at gene body regions. Here, we find that in addition to gene body regions, H3K36me3 is enriched at promoters in primary cells. Through screening, we identify SMYD5, which is recruited to chromatin by RNA polymerase II, as a methyltransferase catalyzing H3K36me3 at promoters. The enzymatic activity of SMYD5 is dependent on its C-terminal glutamic acid-rich domain. Overexpression of full-length Smyd5, but not the C-terminal domain-truncated Smyd5, restores H3K36me3 at promoters in Smyd5 knockout cells. Furthermore, elevated Smyd5 expression contributes to tumorigenesis in liver hepatocellular carcinoma. Together, our findings identify SMYD5 as the H3K36me3 methyltransferase at promoters that regulates gene expression, providing insights into the localization and function of H3K36me3.

| S-EPMC9184575 | biostudies-literature

CpG islands recruit a histone H3 lysine 36 demethylase

Project description:This SuperSeries is composed of the following subset Series: GSE18588: CpG islands recruit a histone H3 lysine 36 demethylase [Illumina sequencing data] GSE21201: CpG islands recruit a histone H3 lysine 36 demethylase [Agilent data] Refer to individual Series

2010-04-26 | E-GEOD-21202 | biostudies-arrayexpress

NSD2 links dimethylation of histone H3 at lysine 36 to oncogenic programming

Project description:This SuperSeries is composed of the following subset Series: GSE29146: NSD2 links dimethylation of histone H3 at lysine 36 to oncogenic programming [ChIP] GSE29147: NSD2 links dimethylation of histone H3 at lysine 36 to oncogenic programming [RNAi] GSE29148: NSD2 links dimethylation of histone H3 at lysine 36 to oncogenic programming [TKO] GSE29150: NSD2 links dimethylation of histone H3 at lysine 36 to oncogenic programming [Transduction] Refer to individual Series

2011-11-29 | E-GEOD-29305 | biostudies-arrayexpress

Histone H3 lysine 27 trimethylation of miRNA genes in HMEC and HMF

Project description:Normal cell type specific histone H3 lysine 27 trimethylation of miRNA genes. HMEC and HMF represent two distinct differentiated cell type present in mammary gland each with a distinct phenotype, a distinct epigenotype as well as distinct miRNA expression pattern. The aim of the study was to determine how epigenetic modifications including histone H3 lysine 27 trimethylation affect miRNA expression. Two cell types HMEC vs. HMF. Biological replicates: 3 pairs of HMEC-HMF of 3 distinct genotypes. Immunoprecipitation using anti-histone H3 trimethylated at lysine 27 (07-449, Millipore).

2011-04-05 | E-GEOD-28376 | biostudies-arrayexpress

Histone H3 lysine 4 trimethylation of miRNA genes in HMEC and HMF

Project description:Normal cell type specific histone H3 lysine 4 trimethylation of miRNA genes. HMEC and HMF represent two distinct differentiated cell type present in mammary gland each with a distinct phenotype, a distinct epigenotype as well as distinct miRNA expression pattern. The aim of the study was to determine how epigenetic modifications including histone H3 lysine 4 trimethylation affect miRNA expression. Two cell types HMEC vs. HMF. Biological replicates: 3 pairs of HMEC-HMF of 3 distinct genotypes. Immunoprecipitation using anti-histone H3 trimethylated at lysine 4 (05-745, Upstate).

2011-04-05 | E-GEOD-28377 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data