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ChIP-seq analysis of histone H3K4me3, H3K27Ac and RNA polymerase II (RNApol II) in HuH-7 cells.

ABSTRACT: ChIP-seq analysis of histone H3K4me3, H3K27Ac and RNA polymerase II (RNApol II) in HuH-7 cells.

PROVIDER: PRJNA431417 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6507240.fastq.gz	Fastqsanger.gz
	SRR6507241.fastq.gz	Fastqsanger.gz
	SRR6507242.fastq.gz	Fastqsanger.gz
	SRR6507243.fastq.gz	Fastqsanger.gz
	SRR6710678.fastq.gz	Fastqsanger.gz

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ChIP-seq analysis of histone H3K4me3, H3K27Ac and RNA polymerase II (RNApol II) in HuH-7 cells.

Project description:The RNA-seq profile of the novel LIN28B variant suggested an alternative transcription initiation (ATI) site approximately 20 kb upstream of LIN28B-WT. Chromatin immunoprecipitation sequencing (ChIP-seq) revealed significant enrichment of histone H3K4me3, H3K27Ac and RNA polymerase II (RNApol II) near the ATI site.

2018-01-25 | GSE109575 | GEO

H3K4me3 regulates RNA polymerase II promoter-proximal pause-release

Project description:Trimethylation of histone H3 lysine 4 (H3K4me3) is associated with transcriptional start sites and proposed to regulate transcription initiation. However, redundant functions of the H3K4 SET1/COMPASS methyltransferase complexes complicate elucidation of the specific role of H3K4me3 in transcriptional regulation. Here, by using mouse embryonic stem cells (mESCs) as a model system, we show that acute ablation of shared subunits of the SET1/COMPASS complexes leads to complete loss of all H3K4 methylation. H3K4me3 turnover occurs more rapidly than H3K4me1 and H3K4me2 and is dependent on KDM5 demethylases. Surprisingly, acute loss of H3K4me3 does not have detectable effects on transcriptional initiation but leads to a widespread decrease in transcriptional output, an increase in RNA polymerase II (RNAPII) pausing and slower elongation. Notably, we show that H3K4me3 is required for the recruitment of the Integrator Complex Subunit 11 (INTS11), which is essential for the eviction of paused RNAPII and transcriptional elongation. Thus, our study demonstrates a distinct role for H3K4me3 in transcriptional pause-release and elongation rather than transcriptional initiation.

2023-02-10 | PXD039176 | Pride

Genome-wide maps of CFP1, RNA Polymerase II and H3K4me3 in mouse brain.

Project description:We report the application of single molecule-based sequencing technology for high-throughput mapping of CFP1, RNA polymerase II and H3K4me3 in mouse brain. By obtaining sequence from chromatin immunoprecipitated DNA, we generated genome-wide binding / chromatin-state maps for mouse brain. We find a good correlation between CFP1 binding and H3K4me3 consistent with it presence in the SetD1 histone methylatransferase complex. Mapped RNA polymerase II colocalised with the majority of CFP1 / H3K4me3 positive CpG islands but not all. This study provides a comprehensive characterisation of the genome wide distribution of a previously uncharacaterised DNA binding factor and suggests a link between DNA base composition and chromatin state. Examination of H3K4me3, RNA PolymeraseII and CFP1 in mouse brain.

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Genome-wide maps of CFP1, RNA Polymerase II and H3K4me3 in mouse brain.

2010-04-15 | GSE18578 | GEO

H3K4me3 and H3K27ac ChIp-seq

Project description:H3K4me3 and H3K27ac ChIp-seq

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ChIP-seq analysis of HeLa cancer stem cells and non-cancer stem cells using Pol II, H3K4me3 and H3K27Ac.

Project description:ChIP-seq analysis of HeLa cancer stem cells and non-cancer stem cells regarding Pol II, H3K4me3 and H3K27Ac.

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Epigenome mapping in quiescent cells reveals a key role for H3K4me3 in regulation of RNA polymerase II activity

Project description:(1) Background: Quiescent cells have stopped dividing and show strongly reduced levels of gene expression during dormancy. In response to appropriate signals the cells can wake up and start growing again. Many histone modifications are regulated in quiescence, but their exact functions remain to be determined. (2) Methods: Here we map the different histone modifications: H3K4me3, H3K9ac, H3K9me2, H3K9me3, and the histone variant H2A.Z, comparing vegetative and quiescent fission yeast (S. pombe) cells. We also map histone H3 as a control and RNA polymerase II (phosphorylated at S2 and S5) to enable comparisons of their occupancies within genes. We use ChIP-seq methodology and several different bioinformatics tools. (3) Results: The histone modification mapping data show that H3K4me3 changes stand out as being the most significant. Changes in occupancy of histone variant H2A.Z was also significant consistent with earlier studies. Regarding gene expression changes in quiescence, we found that changes in mRNA levels were associated with changes in occupancy of RNA polymerase II (S2 and S5). Analysis of quiescence genes showed that increased H3K4me3 levels and RNA polymerase II occupancy was super-significant at a small set of core quiescence genes which are continuously upregulated during dormancy. We demonstrate that several of these genes were require Set1C/COMPASS activity for their strong induction during quiescence. (4) Conclusions: Our results imply that regulation of gene expression in quiescent cells involves epigenome changes with a key role for H3K4me3 in regulation of RNA polymerase II activity, and that different gene activation mechanisms are controlling early and core quiescence genes. Thus, our data give further insights into important epigenome changes in quiescence using fission yeast as experimental model.

2024-10-24 | GSE280066 | GEO

ChIP-seq against RUNX2, RNA-Polymerase II and Histone Marks (H3K27ac, H3K4me1, H3K4me3) in human Papillary Thyroid Cancer cell line (MDA-T41)

Project description:ChIP-seq against RUNX2, RNA-Polymerase II and Histone Marks (H3K27ac, H3K4me1, H3K4me3) in human Papillary Thyroid Cancer cell line (MDA-T41)

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Histone H3 lysine 4 trimethylation regulates RNA polymerase II promoter-proximal pause-release

Project description:Trimethylation of histone H3 lysine 4 (H3K4me3) is associated with transcriptional start sites and proposed to regulate transcription initiation. However, redundant functions of the H3K4 SET1/COMPASS methyltransferase complexes complicate elucidation of the specific role of H3K4me3 in transcriptional regulation. Here, we show that acute ablation of shared subunits of the SET1/COMPASS complexes leads to complete loss of all H3K4 methylation. H3K4me3 turnover occurs more rapidly than H3K4me1 and H3K4me2 and is dependent on KDM5 demethylases. Surprisingly, acute loss of H3K4me3 does not have detectable effects on transcriptional initiation but leads to a widespread decrease in transcriptional output, an increase in RNA polymerase II (RNAPII) pausing and slower elongation. Our study demonstrates a distinct role for H3K4me3 in transcriptional pause-release and elongation rather than transcriptional initiation.

2023-03-14 | PXD028858 | Pride

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