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Phox2b function in the enteric nervous system is conserved in zebrafish and issox10-dependent

Authors
Journal
Mechanisms of Development
0925-4773
Publisher
Elsevier
Publication Date
Volume
122
Issue
5
Identifiers
DOI: 10.1016/j.mod.2004.12.008
Keywords
  • Phox2B
  • Enteric Neuron
  • Colorless
  • Sox10
  • Fate Specification
  • Progenitors
  • Stem Cells
  • Neural Crest
  • Melanophore
Disciplines
  • Medicine

Abstract

Abstract Zebrafish lacking functional sox10 have defects in non-ectomesenchymal neural crest derivatives including the enteric nervous system (ENS) and as such provide an animal model for human Waardenburg Syndrome IV. Here, we characterize zebrafish phox2b as a functionally conserved marker of the developing ENS. We show that morpholino-mediated knockdown of Phox2b generates fish modeling Hirschsprung disease. Using markers, including phox2b, we investigate the ontogeny of the sox10 ENS phenotype. As previously shown for melanophore development, ENS progenitor fate specification fails in these mutant fish. However, in addition, we trace back the sox10 mutant ENS defect to an even earlier time point, finding that most neural crest cells fail to migrate ventrally to the gut primordium.

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