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ChIP-seq analysis of H3K27ac, GATA1 and TAL1 in MYO1D hub vs non-hub enhancer knockout K562 cells

ABSTRACT: Recent studies have highlighted super-enhancers (SEs) as important regulatory elements for gene expression, but their intrinsic properties remain incompletely characterized. Through an integrative analysis of Hi-C and ChIP-seq data, we find that a significant fraction of SEs are hierarchically organized, containing both hub and non-hub enhancers. Hub enhancers share similar histone marks with non-hub enhancers, but are distinctly associated with cohesin and CTCF binding sites and disease-associated genetic variants. Genetic ablation of hub enhancers results in profound defects in gene activation and local chromatin landscape. As such, hub enhancers are the major constituents responsible for SE functional and structural organization.

ORGANISM(S): Homo sapiens

PROVIDER: GSE107726 | GEO | 2018/01/27

REPOSITORIES: GEO

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ChIP-seq analysis of H3K27ac, GATA1 and TAL1 in MYO1D hub vs non-hub enhancer knockout K562 cells

Project description:ChIP-seq analysis of H3K27ac, GATA1 and TAL1 in MYO1D hub vs non-hub enhancer knockout K562 cells

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High-precision mapping of nuclear pore-chromatin interactions reveals new principles of genome organization at the nuclear envelope

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Project description:Diffuse large B-cell lymphoma (DLBCL) is the most common B-cell non-Hodgkin lymphoma and remains incurable in ~40% of patients. Coding-genome sequencing efforts identified several genes/pathways altered in this disease, including new potential therapeutic targets. However, the non-coding genome of DLBCL remains unexplored. Here we show that active superenhancers (SEs) are highly and specifically hypermutated in 99% of DLBCL samples. Such aberrant somatic hypermutation (ASHM) displays signatures of Activation Induced Deaminase activity and is linked to genes encoding B cell developmental regulators and oncogenes. To elucidate the functional consequences of SE-ASHM, we explored two recurrent mutational hotspots identified in the SEs linked to the BCL6 and BCL2 proto-oncogenes, but unmutated in normal GC B cells. These mutations prevent the binding and transcriptional downregulation by the transcriptional repressors BLIMP1 and NR3C1, respectively. Genetic correction of selected mutations restored repressor DNA binding as well as target gene transcriptional repression. Notably, this led to counter-selection of cells harboring corrected alleles, indicating oncogenic dependency from the SE mutations. This pervasive SE mutational mechanism reveals a new major set of genetic lesions deregulating gene expression, which expands the involvement of known oncogenes in DLBCL pathogenesis and identifies new deregulated gene targets of therapeutic relevance.

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