One of the most detailed studies to date of how the interaction between genes and environment results in disease has demonstrated that an inflammatory bowel disease resembling human Crohn's needs a specific mutation, virus, and injury to develop in mice.
Cross section of colon tissue from a
patient with Crohn's disease

Image:Nephron via Wikimedia Commons
"Environmental genomic issues are tough to crack," said linkurl:John Mordes,;http://www.umassmed.edu/igp/faculty/mordes.cfm professor of endocrinology at the University of Massachusetts, who has previously characterized a gene-virus interaction in type1 diabetes. "This is a significant contribution to the evolving understanding of how the environment interacts with genomic predisposition." The team, led by immunologist linkurl:Thaddeus Stappenbeck;http://ddrcc.wustl.edu/FACULTY/Stappenbeck.html and virologist linkurl:Herbert Virgin;http://dbbs.wustl.edu/dbbs/website.nsf/FA/492AFD94078E6ABF86256D4E005B2DE6 of Washington University School of Medicine, found that the diseased state was brought about by the complex interplay among a mutation in an autophagy-related gene called __ATG16L1__, a specific virus, a toxic substance, microbes in the rodent's gut, and...
K. Cadwell, et al., "Virus-Plus-Susceptibility Gene Interaction Determines Crohn's Disease Gene Atg16L1 Phenotypes in Intestine," Cell, 141:1135-45, 2010



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