Format

Send to

Choose Destination
Nat Commun. 2015 Feb 19;6:6178. doi: 10.1038/ncomms7178.

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

Author information

1
Division of Genetics and Epidemiology, The Institute of Cancer Research, Sutton, Surrey SM2 5NG, UK.
2
Division of Molecular Pathology, The Institute of Cancer Research, Sutton, Surrey SM2 5NG, UK.
3
Division of Molecular Pathology, Haemato-Oncology Research Unit, The Institute of Cancer Research, Sutton, Surrey SM2 5NG, UK.
4
Breakthrough Breast Cancer Research Centre, The Institute of Cancer Research, London SW3 6JB, UK.
5
Nuclear Dynamics Programme, The Babraham Institute, Cambridge CB22 3AT, UK.
6
Department of Biosciences and Nutrition, Science for Life Laboratory, Karolinska Institutet, 14 183, Huddinge, Sweden.

Abstract

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.

PMID:
25695508
PMCID:
PMC4346635
DOI:
10.1038/ncomms7178
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Nature Publishing Group Icon for PubMed Central
Loading ...
Support Center