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
-
- Animals
- Cartilage, Articular/embryology
- Enteric Nervous System/cytology
- Enteric Nervous System/embryology
- Face/embryology
- Gene Deletion*
- Humans
- Melanocytes/cytology
- Mesoderm/physiology
- Morphogenesis
- Mosaicism
- Neural Crest/cytology*
- Neural Crest/physiology*
- Neuroglia/cytology
- Neurons/cytology*
- Neurons/physiology
- Neurons, Afferent/cytology
- Pigmentation/genetics
- Zebrafish/embryology*
- Zebrafish/genetics*
- PubMed
- 10631172 Full text @ Development
Citation
Kelsh, R.N. and Eisen, J.S. (2000) The zebrafish colourless gene regulates development of non-ectomesenchymal neural crest derivatives. Development (Cambridge, England). 127(3):515-525.
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
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping