PUBLICATION

The zebrafish colourless gene regulates development of non-ectomesenchymal neural crest derivatives

Authors
Kelsh, R.N. and Eisen, J.S.
ID
ZDB-PUB-000201-29
Date
2000
Source
Development (Cambridge, England)   127(3): 515-525 (Journal)
Registered Authors
Eisen, Judith S., Kelsh, Robert
Keywords
zebrafish; neural crest; cell fate; melanophore; xanthophore; iridophore; neuron; glia
MeSH Terms
  • Melanocytes/cytology
  • Zebrafish/embryology*
  • Zebrafish/genetics*
  • Morphogenesis
  • Humans
  • Neuroglia/cytology
  • Animals
  • Mesoderm/physiology
  • Neurons, Afferent/cytology
  • Cartilage, Articular/embryology
  • Neural Crest/cytology*
  • Neural Crest/physiology*
  • Face/embryology
  • Mosaicism
  • Enteric Nervous System/cytology
  • Enteric Nervous System/embryology
  • Neurons/cytology*
  • Neurons/physiology
  • Gene Deletion*
  • Pigmentation/genetics
(all 20)
PubMed
10631172 Full text @ Development
Abstract
Neural crest forms four major categories of derivatives: pigment cells, peripheral neurons, peripheral glia, and ectomesenchymal cells. Some early neural crest cells generate progeny of several fates. How specific cell fates become specified is still poorly understood. Here we show that zebrafish embryos with mutations in the colourless gene have severe defects in most crest-derived cell types, including pigment cells, neurons and specific glia. In contrast, craniofacial skeleton and medial fin mesenchyme are normal. These observations suggest that colourless has a key role in development of non-ectomesenchymal neural crest fates, but not in development of ectomesenchymal fates. Thus, the cls mutant phenotype reveals a segregation of ectomesenchymal and non-ectomesenchymal fates during zebrafish neural crest development. The combination of pigmentation and enteric nervous system defects makes colourless mutations a model for two human neurocristopathies, Waardenburg-Shah syndrome and Hirschsprung's disease.
Genes / Markers
Figures
Figure Gallery (10 images)
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Expression
Phenotype
Mutations / Transgenics
Allele Construct Type Affected Genomic Region
b4
    Insertion
    t3
      Insertion
      tw2
        Point Mutation
        tw11
          Point Mutation
          1 - 4 of 4
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          Human Disease / Model
          No data available
          Sequence Targeting Reagents
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          Fish
          Antibodies
          Orthology
          No data available
          Engineered Foreign Genes
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          Mapping
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