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Multiple regulatory elements distant from their targets on the linear genome can influence the expression of a single gene through chromatin looping. Chromosome conformation capture implemented in Hi-C allows for genome-wide agnostic characterization of chromatin contacts. However, detection of functional enhancer-promoter interactions is precluded by its effective resolution that is determined by both restriction fragmentation and sensitivity of the experiment. Here we develop a capture Hi-C (cHi-C) approach to allow an agnostic characterization of these physical interactions on a genome-wide scale. Single-nucleotide polymorphisms associated with complex diseases often reside within regulatory elements and exert effects through long-range regulation of gene expression. Applying this cHi-C approach to 14 colorectal cancer risk loci allows us to identify key long-range chromatin interactions in cis and trans involving these loci.

Original publication

DOI

10.1038/ncomms7178

Type

Journal article

Journal

Nature communications

Publication Date

02/2015

Volume

6

Addresses

Division of Genetics and Epidemiology, The Institute of Cancer Research, Sutton, Surrey SM2 5NG, UK.

Keywords

Cell Line, Tumor, Chromosomes, Human, Pair 8, Chromatin, Humans, Colorectal Neoplasms, Genetic Predisposition to Disease, In Situ Hybridization, Fluorescence, Risk Factors, Base Pairing, Statistics as Topic, Genetic Loci, Molecular Sequence Annotation, Nucleotide Motifs