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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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A novel bivalent chromatin state exists at enhancers

ABSTRACT: We assess global chromatin accessibility following 5-Aza-CdR treatment of HCT116 cells Simultaneous genome-wide mapping of DNA methylation and nucleosome occupancy of HCT116 cells

ORGANISM(S): Homo sapiens

SUBMITTER: Jessica Charlet

PROVIDER: E-GEOD-68046 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Bivalent Regions of Cytosine Methylation and H3K27 Acetylation Suggest an Active Role for DNA Methylation at Enhancers.

Charlet Jessica J Duymich Christopher E CE Lay Fides D FD Mundbjerg Kamilla K Dalsgaard Sørensen Karina K Liang Gangning G Jones Peter A PA

Molecular cell 20160501 3

The role of cytosine methylation in the structure and function of enhancers is not well understood. In this study, we investigate the role of DNA methylation at enhancers by comparing the epigenomes of the HCT116 cell line and its highly demethylated derivative, DKO1. Unlike promoters, a portion of regular and super- or stretch enhancers show active H3K27ac marks co-existing with extensive DNA methylation, demonstrating the unexpected presence of bivalent chromatin in both cultured and unculture ...[more]

PMID: 27153539

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The effects of the global loss of DNA methylation on the functional cancer epigenome (Bisulfite-seq)

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A novel bivalent chromatin state exists at enhancers

Project description:We assess global chromatin accessibility following 5-Aza-CdR treatment of HCT116 cells

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Global loss of DNA methylation uncovers intronic enhancers in genes

Project description:We used HCT116 colorectal cancer cells with and without mutations in DNA methyltransferases (resulting in a 95% reduction in global DNA methylation levels) to study the relationship between DNA methylation, histone modifications, and gene expression. (The double knockout cell line is called DKO1) Examination of DNA methylation, two histone modifications, RNA polymerase II ChIP-seq and RNA expression in two cell line (HCT116 and DKO1). One of relipates of HCT116 RNA P II ChIP-seq is from GSM970210. Histone modification data(H3K27ac, H3K4me3) of HCT116 are from GSM945304, GSE31755. Two replicates of RNA-seq data in HCT116 are from GSM1266733 and GSM1266734

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Project description:Histone H3 lysine 4 (H3K4) can be mono-, di-, and trimethylated by members of the COMPASS (COMplex of Proteins ASsociated with Set1) family from yeast to human and these modifications can be found at distinct regions of the genome. Monomethylation of histone H3K4 (H3K4me1) is relatively more enriched at metazoan enhancer regions compared to trimethylated histone H3K4 (H3K4me3), which are found at transcription start sites in all eukaryotes. Our recent studies in Drosophila demonstrated that the Trithorax-related (Trr) branch of the COMPASS family regulates enhancer activity and is responsible for the implementation of H3K4me1 at these regions. There are six COMPASS family members in mammals, two of which, MLL3 and MLL4, are most closely related to Drosophila Trr. Here, we use ChIP-seq of this class of COMPASS family members in both human HCT116 cells and mouse embryonic stem cells and find that MLL4 is preferentially found at enhancer regions. MLL3 and MLL4 are frequently mutated in cancer, and indeed, the widely used HCT116 cancer cell line contains inactivating mutations in the MLL3 gene. Using HCT116 cells in which MLL4 has also been knocked out, we demonstrate that MLL4 is a major regulator of H3K4me1 in these cells, with the greatest loss of monomethylation at enhancer regions. Moreover, we found a redundant role between Mll3 and Mll4 in enhancer H3K4 monomethylation in mouse embryonic fibroblast (MEF) cells. These findings suggest that mammalian MLL3/MLL4 function in the regulation of enhancer activity and enhancer-promoter communication during gene expression and that mutations of MLL3 and MLL4 found in cancer could exert their properties through enhancer malfunction. ChIP-Seq in mouse embryonic stem (mES) cells for MLL4. ChIP-seq of MLL4 and p300 in human parental HCT116 cells. ChIP-seq of H3K4me1, H3K4me2 and H3K4me3 in parental HCT116 cells and HCT116 cells with Mll4∆set.

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