ZFIN ID: ZDB-PUB-130211-13
Kit signaling is involved in melanocyte stem cell fate decisions in zebrafish embryos
O'Reilly-Pol, T., and Johnson, S.L.
Date: 2013
Source: Development (Cambridge, England)   140(5): 996-1002 (Journal)
Registered Authors: Johnson, Stephen L., O'Reilly-Pol, Thomas
Keywords: Clonal analysis, Fate determination, KIT, Melanocyte, Regeneration, Stem cell
MeSH Terms:
  • Animals
  • Animals, Genetically Modified
  • Cell Differentiation/genetics*
  • Cell Proliferation
  • Cell Survival/genetics
  • Clonal Evolution/genetics
  • Embryo, Nonmammalian
  • Embryonic Stem Cells/metabolism
  • Embryonic Stem Cells/physiology*
  • Gene Dosage/physiology
  • Melanocytes/metabolism
  • Melanocytes/physiology*
  • Models, Biological
  • Proto-Oncogene Proteins c-kit/genetics
  • Proto-Oncogene Proteins c-kit/metabolism
  • Proto-Oncogene Proteins c-kit/physiology*
  • Regeneration/genetics
  • Regeneration/physiology
  • Signal Transduction/genetics
  • Signal Transduction/physiology
  • Stem Cell Factor/genetics
  • Stem Cell Factor/metabolism
  • Stem Cell Factor/physiology
  • Zebrafish/embryology*
  • Zebrafish/genetics
  • Zebrafish/physiology
PubMed: 23364331 Full text @ Development

Adult stem cells are crucial for growth, homeostasis and repair of adult animals. The melanocyte stem cell (MSC) and melanocyte regeneration is an attractive model for studying regulation of adult stem cells. The process of melanocyte regeneration can be divided into establishment of the MSC, recruitment of the MSC to produce committed daughter cells, and the proliferation, differentiation and survival of these daughter cells. Reduction of Kit signaling results in dose-dependent reduction of melanocytes during larval regeneration. Here, we use clonal analysis techniques to develop assays to distinguish roles for these processes during zebrafish larval melanocyte regeneration. We use these clonal assays to investigate which processes are affected by the reduction in Kit signaling. We show that the regeneration defect in kita mutants is not due to defects in MSC recruitment or in the proliferation, differentiation or survival of the daughter cells, but is instead due to a defect in stem cell establishment. Our analysis suggests that the kit MSC establishment defect results from inappropriate differentiation of the MSC lineage.