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

Cherie Rao, Dorothee Foernzler, Stacie K. Loftus, Shanming Liu, John Douglas Mcpherson, Katherine A. Jungers, Suneel S. Apte, William J. Pavan, David R. Beier

Research output: Contribution to journalArticle

62 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)4665-4672
Number of pages8
JournalDevelopment
Volume130
Issue number19
DOIs
StatePublished - Oct 2003
Externally publishedYes

Keywords

  • ADAMTS
  • Melanocyte migration
  • Mouse
  • White-spotting

ASJC Scopus subject areas

  • Molecular Biology
  • Developmental Biology

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    Rao, C., Foernzler, D., Loftus, S. K., Liu, S., Mcpherson, J. D., Jungers, K. A., Apte, S. S., Pavan, W. J., & Beier, D. R. (2003). A defect in a novel ADAMTS family member is the cause of the belted white-spotting mutation. Development, 130(19), 4665-4672. https://doi.org/10.1242/dev.00668