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Capture Hi-C identifies the chromatin interactome of colorectal cancer risk loci

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Roland Ja¨ger, Gabriele Migliorini, Marc Henrion, Radhika Kandaswamy, Helen E. Speedy, Andreas Heindl, Nicola Whiffin, Maria J. Carnicer, Laura Broome, Nicola H. Dryden, Takashi Nagano, Stefan Schoenfelder, Martin Enge, Yinyin Yuan, Jussi Taipale, Peter Fraser, Olivia Fletcher, Richard S. Houlston

Original languageEnglish
Article number6178
JournalNature Communications
Early online date19 Feb 2015
Accepted/In press30 Dec 2014
E-pub ahead of print19 Feb 2015


King's Authors


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.

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