Steel Factor Directs Melanocyte Development In-Vitro Through Selective Regulation of the Number of C-Kit(+) Progenitors

Reid, K, Nishikawa, SI, Bartlett, PF and Murphy, M (1995) Steel Factor Directs Melanocyte Development In-Vitro Through Selective Regulation of the Number of C-Kit(+) Progenitors. Developmental Biology, 169 2: 568-579. doi:10.1006/dbio.1995.1170


Author Reid, K
Nishikawa, SI
Bartlett, PF
Murphy, M
Title Steel Factor Directs Melanocyte Development In-Vitro Through Selective Regulation of the Number of C-Kit(+) Progenitors
Journal name Developmental Biology   Check publisher's open access policy
ISSN 0012-1606
Publication date 1995-06-01
Year available 1995
Sub-type Article (original research)
DOI 10.1006/dbio.1995.1170
Open Access Status Not yet assessed
Volume 169
Issue 2
Start page 568
End page 579
Total pages 12
Place of publication SAN DIEGO
Publisher ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS
Language eng
Abstract Studies of mice containing mutations in the genes for a receptor tyrosine kinase, c-kit, or its cognate ligand, Steel factor (SLF), establish that this signaling pathway is required for the development of melanocytes from their precursors in the embryonic neural crest (NC). In order to define the mechanism of this requirement, we have labeled cells expressing c-kit with an anti-c-kit antibody (ACK2) and studied the action of SLP on these cells in cultures of murine trunk NC. c-kit positive (c-kit(+)) cells first appeared after 2 days in culture and were morphologically indistinguishable from other NC cells. These cells subsequently expressed tyrosinase-related protein, an early marker for the melanocyte lineage, and became pigmented in the presence of a phorbol ester. Further, elimination of the c-kit(+) population, by incubating the cultures in ACK2, resulted in the ablation of the melanocyte population, but had no effect on the generation of other neural crest derivatives. These data indicate that c-kit(+) cells arising from the neural crest are melanocyte progenitors. The addition of SLF to these cultures stimulated an increase in the number of c-kit(+) cells, and further studies indicated that SLF acts as both a survival and a proliferative factor for c-kit(+) cells. These findings provide a mechanism of regulation of melanocyte development, whereby c-kit is exclusively expressed by melanocyte progenitors within the neural crest precursor population, and subsequent survival and proliferation of these progenitors is regulated by SLF. (C) 1995 Academic Press,Inc.
Keyword Tyrosinase-Related Protein
Leukemia Inhibitory Factor
Crest-Derived Cells
C-Kit Receptor
Growth-Factor
Neural Crest
W-Locus
Si-Locus
Kinase Receptor
Mouse
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Unknown

Document type: Journal Article
Sub-type: Article (original research)
Collection: ResearcherID Downloads - Archived
 
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