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ChIP-seq for CTCF, H3K4me3 and H3K27ac following CTCF RNAi in LNCaP cells and IMR90 cells

ABSTRACT: This study aimed to ascertain the effect of CTCF RNAi on gene expression, chromatin conformation and the chromatin environment in prostate cancer cell line, LNCaP This study aimed to confirm loss of CTCF sites following CTCF RNAi in IMR90 cells

ORGANISM(S): Homo sapiens

PROVIDER: GSE125639 | GEO | 2019/11/18

REPOSITORIES: GEO

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ChIP-seq for CTCF, H3K4me3 and H3K27ac following CTCF RNAi in LNCaP cells and IMR90 cells

Project description:ChIP-seq for CTCF, H3K4me3 and H3K27ac following CTCF RNAi in LNCaP cells and IMR90 cells

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Expression data from CTCF RNAi experiments in LNCaP cell line

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Project description:Background. Recent epigenomic studies have shown that the length of a DNA region covered by an epigenetic mark is not just a byproduct of the assaying technologies and has functional implications for that locus. For example, expanded regions of DNA sequences that are marked by enhancer-specific histone modifications, such as acetylation of histone H3 lysine 27 (H3K27ac) domains coincide with cell-specific enhancers, known as super or stretch enhancers. Similarly, promoters of genes critical for cell-specific functions are marked by expanded H3K4me3 domains in the cognate cell type, and these can span DNA regions from 4-5kb up to 40-50kb in length. These expanded H3K4me3 domains are known as buffer domains or super promoters. Methods. To ask what correlates with-and potentially regulates-the length of loci marked with these two important histone marks, H3K4me3 and H3K27ac, we built Random Forest regression models. With these models, we computationally identified genomic and epigenomic patterns that are predictive for the length of these marks in seven ENCODE cell lines. Results. We found that certain epigenetic marks and transcription factors explain the variability of the length of H3K4me3 and H3K27ac marks across different cell types, which implies that the lengths of these two epigenetic marks are tightly regulated in a given cell type. Our source code for the regression models and data can be found at our GitHub page: https://github.com/zubekj/broad_peaks. Discussion. Our Random Forest based regression models enabled us to estimate the individual contribution of different epigenetic marks and protein binding patterns to the length of H3K4me3 and H3K27ac deposition patterns, therefore potentially revealing genomic signatures at cell specific regulatory elements.

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