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First published online August 18, 2003
doi: 10.1242/10.1242/dev.00668

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Development 130, 4665-4672 (2003)
Copyright © 2003 The Company of Biologists Limited

A defect in a novel ADAMTS family member is the cause of the belted white-spotting mutation

Cherie Rao1,*, Dorothee Foernzler1,*, Stacie K. Loftus2, Shanming Liu1, John D. McPherson3, Katherine A. Jungers4, Suneel S. Apte4, William J. Pavan2 and David R. Beier1,*,{dagger}

1 Genetics Division, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02476, USArr
2 National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 02115, USA
3 Department of Genetics, Washington University, St. Louis, MO 20892, USA
4 Department of Biomedical Engineering, Cleveland Clinic Foundation, Cleveland, OH 44195, USA

{dagger} Author for correspondence (e-mail: beier{at}rascal.med.harvard.edu)

Accepted 22 May 2003

Several features of the pigment defect in belted (bt) mutant mice suggest that it occurs as a result of a defect in melanocyte development that is unique from those described for other classical white-spotting mutations. We report here that bt mice carry mutations in Adamts20, a novel member of the ADAMTS family of secreted metalloproteases. Adamts20 shows a highly dynamic pattern of expression in the developing embryo that generally precedes the appearance of melanoblasts in the same region, and is not expressed in the migrating cells themselves. Adamts20 shows remarkable homology with GON-1, an ADAMTS family protease required for distal tip cell migration in C. elegans. Our results suggest that the role of ADAMTS proteases in the regulation of cell migration has been conserved in mammalian development.

Key words: ADAMTS, White-spotting, Melanocyte migration, Mouse


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© The Company of Biologists Ltd 2003