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Enhancer connectome in primary human cells reveals target genes of disease-associated DNA elements

ABSTRACT: Enhancer connectome in primary human cells reveals target genes of disease-associated DNA elements

PROVIDER: PRJNA394682 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5831480_1.fastq.gz	Fastqsanger.gz
	SRR5831480_2.fastq.gz	Fastqsanger.gz
	SRR5831490_1.fastq.gz	Fastqsanger.gz
	SRR5831490_2.fastq.gz	Fastqsanger.gz
	SRR5831500_1.fastq.gz	Fastqsanger.gz

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Enhancer connectome in primary human cells reveals target genes of disease-associated DNA elements

Project description:The imprecision of linking intergenic mutations to target genes has limited molecular understanding of diverse human diseases. Here, we show H3K27ac HiChIP generates high-resolution contact maps of active enhancers and target genes in rare primary human T cell subtypes and coronary artery smooth muscle cells. Differentiation of naïve T cells to either T helper 17 cells or regulatory T cells create subtype-specific enhancer-promoter interactions, specifically at regions of shared DNA accessibility. We provide an atlas for assigning molecular functions to autoimmune and cardiovascular disease risk variants, linking hundreds of noncoding variants to putative gene targets. HiChIP target genes are supported by CRISPR interference and activation of enhancers, expression quantitative trait loci, and allele-specific enhancer loops in patient-derived primary cells. The majority of disease-associated enhancers contact genes beyond the nearest gene in the linear genome, leading to a four-fold expansion of target genes for autoimmune and cardiovascular diseases.

2017-08-28 | GSE101498 | GEO

Enhancer connectome in primary human cells identifies target genes of disease-associated DNA elements.

Project description:The challenge of linking intergenic mutations to target genes has limited molecular understanding of human diseases. Here we show that H3K27ac HiChIP generates high-resolution contact maps of active enhancers and target genes in rare primary human T cell subtypes and coronary artery smooth muscle cells. Differentiation of naive T cells into T helper 17 cells or regulatory T cells creates subtype-specific enhancer-promoter interactions, specifically at regions of shared DNA accessibility. These data provide a principled means of assigning molecular functions to autoimmune and cardiovascular disease risk variants, linking hundreds of noncoding variants to putative gene targets. Target genes identified with HiChIP are further supported by CRISPR interference and activation at linked enhancers, by the presence of expression quantitative trait loci, and by allele-specific enhancer loops in patient-derived primary cells. The majority of disease-associated enhancers contact genes beyond the nearest gene in the linear genome, leading to a fourfold increase in the number of potential target genes for autoimmune and cardiovascular diseases.

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CRISPR enhancer scan to detect critical elements for the regulation of EVI1 in a translocated enhancer

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Enhancer Cis Elements Instruct Promoter-Enhancer Interaction, Promoter-Enhancer Insulation and Compartmental Segregation

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Project description:BruUV-seq utilizes UV light to introduce transcription-blocking DNA lesions randomly in the genome prior to bromouridine-labeling and deep sequencing of nascent RNA. By inhibiting transcription elongation, but not initiation, pre-treatment with UV light leads to a redistribution of transcription reads resulting in the enhancement of nascent RNA signal towards the 5â²-end of genes promoting the identification of transcription start sites (TSSs). Furthermore, transcripts associated with arrested RNA polymerases are protected from 3â²â5â² degradation and thus, unstable transcripts such as putative enhancer RNA (eRNA) are dramatically increased. Validation of BruUV-seq against GRO-cap that identifies capped run-on transcripts showed that most BruUV-seq peaks overlapped with GRO-cap signal over both TSSs and enhancer elements. Finally, BruUV-seq identified putative enhancer elements induced by tumor necrosis factor (TNF) treatment concomitant with expression of nearby TNF-induced genes. Taken together, BruUV-seq is a powerful new approach for identifying TSSs and active enhancer elements genome-wide in intact cells. Two cell lines were used. K562 cells were mock-irradiated (control) or UVC-irradiated at two different doses (25 and 100 J/m^2). HF1 cells were UVC-irradiated (20 J/m^2) in three independent experiments (nfUV4,nfUV3a, and nfUV3b). In one experiment, HF1 cells were also treated with TNF (10 ng/mL) 1 h prior to UV irradiation (tnfpreUV2, paired with nfUV4).

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