PMID- 8806824
OWN - NLM
STAT- MEDLINE
DCOM- 19961024
LR  - 20091119
IS  - 0012-1606 (Print)
IS  - 0012-1606 (Linking)
VI  - 177
IP  - 2
DP  - 1996 Aug 1
TI  - Ectopic c-kit expression affects the fate of melanocyte precursors in Patch 
      mutant embryos.
PG  - 463-74
AB  - The Patch (Ph) mutation in the mouse, a deletion that includes the gene for PDGFR 
      alpha, is a recessive lethal that exhibits a dominant pigment phenotype in 
      heterozygotes. To assess whether the Ph mutation acts cell-autonomously or 
      non-autonomously on melanocyte development, we have examined the melanogenic 
      potential of neural crest populations from normal and mutant crest cells in vitro 
      and the pattern of dispersal and survival of melanocyte precursors (MPs) in vivo. 
      We report that trunk neural crest cells from homozygous Ph embryos give rise to 
      pigmented melanocytes in vitro in response to Steel factor (SlF). In vivo, 
      homozygous Ph embryos contain a subpopulation of crest-derived cells that express 
      c-kit and tyrosinase-related protein-2 characteristic of MPs. These cells begin 
      to migrate normally on the lateral crest migration pathway, but then fail to 
      disperse in the dermal mesenchyme and subsequently disappear. Although dermal 
      mesenchyme is adversely affected in Ph homozygotes, SlF mRNA expression by the 
      cells of the dermatome is normal in Ph embryos when neural crest-derived MPs 
      start to migrate on the lateral pathway. In contrast, mRNA for the SlF receptor, 
      c-kit, was observed to be ectopically expressed in somites and lateral mesenchyme 
      in embryos carrying the Ph mutation. Based on this ectopic expression of c-kit in 
      Ph mutant embryos, and the observed distribution of SlF protein in normal and 
      mutant embryos, we suggest that competition for limited amounts of SlF localized 
      on the lateral neural crest migration pathway alters melanocyte dispersal and 
      survival.
FAU - Wehrle-Haller, B
AU  - Wehrle-Haller B
AD  - Institute of Neuroscience, University of Oregon, Eugene 97403-1254, USA.
FAU - Morrison-Graham, K
AU  - Morrison-Graham K
FAU - Weston, J A
AU  - Weston JA
LA  - eng
GR  - DE-04316/DE/NIDCR NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Dev Biol
JT  - Developmental biology
JID - 0372762
RN  - 0 (Melanins)
RN  - 0 (RNA, Messenger)
RN  - 0 (Stem Cell Factor)
RN  - EC 2.7.10.1 (Proto-Oncogene Proteins c-kit)
SB  - IM
MH  - Animals
MH  - Base Sequence
MH  - Cell Movement
MH  - Cells, Cultured
MH  - Female
MH  - Gene Deletion
MH  - Gene Expression Regulation, Developmental
MH  - Male
MH  - Melanins/biosynthesis
MH  - Melanocytes/*physiology
MH  - Mice/*embryology
MH  - Mice, Inbred BALB C
MH  - Mice, Inbred C57BL
MH  - Molecular Sequence Data
MH  - Neural Crest/cytology
MH  - Pregnancy
MH  - Proto-Oncogene Proteins c-kit/analysis/*biosynthesis/genetics
MH  - RNA, Messenger/analysis
MH  - Stem Cell Factor/physiology
MH  - Stem Cells
EDAT- 1996/08/01 00:00
MHDA- 1996/08/01 00:01
CRDT- 1996/08/01 00:00
PHST- 1996/08/01 00:00 [pubmed]
PHST- 1996/08/01 00:01 [medline]
PHST- 1996/08/01 00:00 [entrez]
AID - S0012-1606(96)90178-5 [pii]
AID - 10.1006/dbio.1996.0178 [doi]
PST - ppublish
SO  - Dev Biol. 1996 Aug 1;177(2):463-74. doi: 10.1006/dbio.1996.0178.