Phenotype of mice lacking functional Deleted in colorectal cancer (Dec) gene

Amin Fazeli, Stephanie L. Dickinson, Michelle L. Hermiston, Robert V. Tighe, Robert G. Steen, Clayton G. Small, Esther T. Stoeckli, Kazuko Keino-Masu, Masayuki Masu, Helen Rayburn, Jonathan Simons, Roderick T. Bronson, Jeffrey I. Gordon, Marc Tessier-Lavigne and Robert A. Weinberg
Additional contact information
Amin Fazeli: Massachusetts Institute of Technology
Stephanie L. Dickinson: Massachusetts Institute of Technology
Michelle L. Hermiston: Washington University School of Medicine
Robert V. Tighe: Massachusetts Institute of Technology
Robert G. Steen: Massachusetts Institute of Technology/Whitehead Institute Genome Center
Clayton G. Small: Massachusetts Institute of Technology
Esther T. Stoeckli: Developmental Biology and Neuroscience, University of California
Kazuko Keino-Masu: Developmental Biology and Neuroscience, University of California
Masayuki Masu: Developmental Biology and Neuroscience, University of California
Helen Rayburn: Massachusetts Institute of Technology
Jonathan Simons: Johns Hopkins University
Roderick T. Bronson: Tufts University Schools of Medicine and Veterinary Medicine
Jeffrey I. Gordon: Washington University School of Medicine
Marc Tessier-Lavigne: Developmental Biology and Neuroscience, University of California
Robert A. Weinberg: Massachusetts Institute of Technology

Nature, 1997, vol. 386, issue 6627, 796-804

Abstract: Abstract The DCC (Deleted in colorectal cancer) gene was first identified as a candidate for a tumour-suppressor gene on human chromosome 18q. More recently, in vitro studies in rodents have provided evidence that DCC might function as a receptor for the axonal chemoattractant netrin-1. Inactivation of the murine Dcc gene caused defects in axonal projections that are similar to those observed in netrin-1-deficient mice but did not affect growth, differentiation, morphogenesis or tumorigenesis in mouse intestine. These observations fail to support a tumour-suppressor function for Dcc, but are consistent with the hypothesis that DCC is a component of a receptor for netrin-1.

Date: 1997
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DOI: 10.1038/386796a0

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