Fine-mapping inflammatory bowel disease loci to single-variant resolution View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2017-06-28

AUTHORS

Hailiang Huang, Ming Fang, Luke Jostins, Maša Umićević Mirkov, Gabrielle Boucher, Carl A. Anderson, Vibeke Andersen, Isabelle Cleynen, Adrian Cortes, François Crins, Mauro D’Amato, Valérie Deffontaine, Julia Dmitrieva, Elisa Docampo, Mahmoud Elansary, Kyle Kai-How Farh, Andre Franke, Ann-Stephan Gori, Philippe Goyette, Jonas Halfvarson, Talin Haritunians, Jo Knight, Ian C. Lawrance, Charlie W. Lees, Edouard Louis, Rob Mariman, Theo Meuwissen, Myriam Mni, Yukihide Momozawa, Miles Parkes, Sarah L. Spain, Emilie Théâtre, Gosia Trynka, Jack Satsangi, Suzanne van Sommeren, Severine Vermeire, Ramnik J. Xavier, Rinse K. Weersma, Richard H. Duerr, Christopher G. Mathew, John D. Rioux, Dermot P. B. McGovern, Judy H. Cho, Michel Georges, Mark J. Daly, Jeffrey C. Barrett

ABSTRACT

Inflammatory bowel diseases are chronic gastrointestinal inflammatory disorders that affect millions of people worldwide. Genome-wide association studies have identified 200 inflammatory bowel disease-associated loci, but few have been conclusively resolved to specific functional variants. Here we report fine-mapping of 94 inflammatory bowel disease loci using high-density genotyping in 67,852 individuals. We pinpoint 18 associations to a single causal variant with greater than 95% certainty, and an additional 27 associations to a single variant with greater than 50% certainty. These 45 variants are significantly enriched for protein-coding changes (n = 13), direct disruption of transcription-factor binding sites (n = 3), and tissue-specific epigenetic marks (n = 10), with the last category showing enrichment in specific immune cells among associations stronger in Crohn’s disease and in gut mucosa among associations stronger in ulcerative colitis. The results of this study suggest that high-resolution fine-mapping in large samples can convert many discoveries from genome-wide association studies into statistically convincing causal variants, providing a powerful substrate for experimental elucidation of disease mechanisms. More... »

PAGES

173-178

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  • Journal

    TITLE

    Nature

    ISSUE

    7662

    VOLUME

    547

    Author Affiliations

  • Broad Institute of MIT and Harvard, 02141, Cambridge, Massachusetts, USA
  • Faculty of Veterinary Medicine, University of Liège, 4000, Liège, Belgium
  • Christ Church, University of Oxford, OX1 1DP, St Aldates, UK
  • Wellcome Trust Sanger Institute, Wellcome Genome Campus, CB10 1SA, Hinxton, Cambridgeshire, UK
  • Research Center, Montreal Heart Institute, H1T 1C8, Montréal, Québec, Canada
  • Institute of Molecular Medicine, University of Southern Denmark, 5000, Odense, Denmark
  • Department of Human Genetics, 3000, KU Leuven, Leuven, Belgium
  • Nuffield Department of Clinical Neurosciences, Division of Clinical Neurology, Oxford Centre for Neuroinflammation, John Radcliffe Hospital, University of Oxford, OX3 9DS, Oxford, UK
  • IKERBASQUE, Basque Foundation for Science, 48013, Bilbao, Spain
  • Illumina, 92122, San Diego, California, USA
  • Institute of Clinical Molecular Biology, Christian-Albrechts-University of Kiel, 24118, Kiel, Germany
  • Department of Gastroenterology, Faculty of Medicine and Health, Örebro University, SE-70182, Örebro, Sweden
  • F. Widjaja Foundation Inflammatory Bowel and Immunobiology Research Institute, Cedars-Sinai Medical Center, 90048, Los Angeles, California, USA
  • Data Science Institute and Lancaster Medical School, Lancaster University, LA1 4YG, Lancaster, UK
  • Harry Perkins Institute for Medical Research, School of Medicine and Pharmacology, University of Western Australia, 6150, Murdoch, Western Australia, Australia
  • Gastrointestinal Unit, Western General Hospital University of Edinburgh, Edinburgh, UK
  • Division of Gastroenterology, Centre Hospitalier Universitaire (CHU) de Liège, 4000, Liège, Belgium
  • Institute of Livestock and Aquacultural Sciences, Norwegian University of Life Sciences, 1430 Ås, Norway
  • Laboratory for Genotyping Development, Center for Integrative Medical Sciences, RIKEN, 230-0045, Yokohama, Kanagawa, Japan
  • Inflammatory Bowel Disease Research Group, Addenbrooke’s Hospital, CB2 0QQ, Cambridge, UK
  • Open Targets, Wellcome Trust Genome Campus, CB10 1SD, Hinxton, Cambridgeshire, UK
  • Department of Gastroenterology and Hepatology, University of Groningen and University Medical Center Groningen, 9700RB, Groningen, The Netherlands
  • Division of Gastroenterology, University Hospital Gasthuisberg, 3000, Leuven, Belgium
  • Gastroenterology Unit, Massachusetts General Hospital, Harvard Medical School, 02114, BostonMassachusetts, USA
  • Department of Human Genetics, University of Pittsburgh Graduate School of Public Health, 15261, Pittsburgh, Pennsylvania, USA
  • Sydney Brenner Institute for Molecular Bioscience, University of the Witwatersrand, 2193, Johannesburg, South Africa
  • Faculté de Médecine, Université de Montréal, H3C 3J7, Montréal, Québec, Canada
  • Department of Genetics, Yale School of Medicine, 06510, New Haven, Connecticut, USA
  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/nature22969

    DOI

    http://dx.doi.org/10.1038/nature22969

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1090278096

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/28658209


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