A defect in a novel ADAMTS family member is the cause of the belted white-spotting mutation-Reference-Cited by-同舟云学术

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

Published:2003-10-01 Issue:19 Volume:130 Page:4665-4672
ISSN:1477-9129
Container-title:Development
language:en
Short-container-title:

Author:

Rao Cherie¹,Foernzler Dorothee¹,Loftus Stacie K.²,Liu Shanming¹,McPherson John D.³,Jungers Katherine A.⁴,Apte Suneel S.⁴,Pavan William J.²,Beier David R.¹

Affiliation:

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

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.

Publisher

The Company of Biologists

Subject

Developmental Biology,Molecular Biology

Link

http://journals.biologists.com/dev/article-pdf/130/19/4665/1144632/4665.pdf

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