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A genome-wide association scan of nonsynonymous SNPs identifies a susceptibility variant for Crohn disease in ATG16L1. 2007
Jochen Hampe, and
Andre Franke, and
Philip Rosenstiel, and
Andreas Till, and
Markus Teuber, and
Klaus Huse, and
Mario Albrecht, and
Gabriele Mayr, and
Francisco M De La Vega, and
Jason Briggs, and
Simone Günther, and
Natalie J Prescott, and
Clive M Onnie, and
Robert Häsler, and
Bence Sipos, and
Ulrich R Fölsch, and
Thomas Lengauer, and
Matthias Platzer, and
Christopher G Mathew, and
Michael Krawczak, and
Stefan Schreiber
Institute for Clinical Molecular Biology, Christian-Albrechts University Kiel, University Hospital Schleswig-Holstein, 24105 Kiel, Germany. jhampe@1med.uni-kiel.de
We performed a genome-wide association study of 19,779 nonsynonymous SNPs in 735 individuals with Crohn disease and 368 controls. A total of 7,159 of these SNPs were informative. We followed up on all 72 SNPs with P <or= 0.01 with an allele-based disease association test in 380 independent Crohn disease trios, 498 Crohn disease singleton cases and 1,032 controls. Disease association of rs2241880 in the autophagy-related 16-like 1 gene (ATG16L1) was replicated in these samples (P = 4.0 x 10(-8)) and confirmed in a UK case-control sample (P = 0.0004). By haplotype and regression analysis, we found that marker rs2241880, a coding SNP (T300A), carries virtually all the disease risk exerted by the ATG16L1 locus. The ATG16L1 gene encodes a protein in the autophagosome pathway that processes intracellular bacteria. We found a statistically significant interaction with respect to Crohn disease risk between rs2241880 and the established CARD15 susceptibility variants (P = 0.039). Together with the lack of association between rs2241880 and ulcerative colitis (P > 0.4), these data suggest that the underlying biological process may be specific to Crohn disease.
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