Researchers Put Linkage Disequilibrium on the Map

Image © Nature  MUTATION AND TRUNCATION: These DNA sequence electropherograms show a patient from "family 7" who is homozygous for a cytosine c insertion, as indicated by the arrow. The mutation encodes a truncated NOD2 protein. (Reprinted with permission from Nature, 411:603-6, 2001.) After years of failed promises that researchers would find genes linked to cancers, heart disease, and other complex human ailments, two independent research teams, using different approaches, localiz

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After years of failed promises that researchers would find genes linked to cancers, heart disease, and other complex human ailments, two independent research teams, using different approaches, localized a gene on human chromosome 16 that increases susceptibility to Crohn disease. One team was led by Gilles Thomas, Fondation Jean Dausset-CEPH, Paris; the other was led by Gabriel Nuñez, University of Michigan Medical School, and Judy Cho, University of Chicago Hospitals. The scientists described these 2001 discoveries in back-to-back Nature papers, two of this issue's three Hot Papers.1,2

The Nuñez team, using a classical candidate gene approach, discerned that the NOD2 gene, which plays a role in recognizing bacteria, is faulty in patients with Crohn disease. This discovery suggests that the disease is partially caused by an innate immune response to bacteria. The Thomas team's findings championed positional, or linkage disequilibrium (LD) mapping, a statistical approach to finding disease genes.

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