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H3K4me3 Marks in Normal and Cancerous Prostate Cells

ABSTRACT: H3K4me3 ChIP-seq was done to examine transcription start sites in a genome wide manner, and compare results to CAGE-seq

ORGANISM(S): Homo sapiens

PROVIDER: GSE38682 | GEO | 2012/11/30

SECONDARY ACCESSION(S): PRJNA168463

REPOSITORIES: GEO

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H3K4me3 Marks in Normal and Cancerous Prostate Cells

Project description:H3K4me3 ChIP-seq was done to examine transcription start sites in a genome wide manner, and compare results to CAGE-seq One PrEC sample, a normal cell line. One LNCaP sample, a cancer cell line.

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Normal and Cancerous Prostate Cells

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Project description:The histone modification H3K27me3 is representative of silenced regions of the genome. Changes between the normal and cancer state were investigated.

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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.

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Project description:The data depicts H3k4me3-CHIP SEQ results done on WM164 cells before treatment and after 50 days treatment with Dabrafenib

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