PUBLICATION
Skeletal and pigment cell defects in the lockjaw mutant reveal multiple roles for zebrafish tfap2a in neural crest development
- Authors
- Knight, R.D., Javidan, Y., Nelson, S., Zhang, T., and Schilling, T.
- ID
- ZDB-PUB-040109-21
- Date
- 2004
- Source
- Developmental Dynamics : an official publication of the American Association of Anatomists 229(1): 87-98 (Journal)
- Registered Authors
- Knight, Robert, Nelson, Sarah, Schilling, Tom, Zhang, Tiantian
- Keywords
- Danio rerio, craniofacial, pigment, kit, AP-2, Hox
- MeSH Terms
-
- Animals
- Biological Evolution
- Body Patterning/genetics
- Bone Development/genetics
- Branchial Region/cytology
- Branchial Region/embryology
- Branchial Region/metabolism
- Cell Movement/genetics
- Gene Expression Regulation, Developmental
- Genes, Homeobox
- In Situ Hybridization
- Melanocytes/cytology
- Melanocytes/metabolism
- Models, Biological
- Mutation
- Neural Crest/cytology*
- Neural Crest/embryology*
- Neural Crest/metabolism
- Zebrafish/embryology*
- Zebrafish/genetics*
- Zebrafish/metabolism
- PubMed
- 14699580 Full text @ Dev. Dyn.
Citation
Knight, R.D., Javidan, Y., Nelson, S., Zhang, T., and Schilling, T. (2004) Skeletal and pigment cell defects in the lockjaw mutant reveal multiple roles for zebrafish tfap2a in neural crest development. Developmental Dynamics : an official publication of the American Association of Anatomists. 229(1):87-98.
Abstract
Members of the AP-2 transcription factor family have critical roles in many aspects of embryonic development. The zebrafish tfap2a mutant lockjaw (low) displays defects in skeletal and pigment cell derivatives of the neural crest. Here we show essential roles for tfap2a in subsets of embryonic cartilages and pigment cells. Defects in cartilage of the hyoid arch in low correlate with a loss of Hox group 2 gene expression and are suggestive of a transformation to a mandibular fate. In contrast, loss of joints in the mandibular arch and defects in certain types of pigment cells suggest a requirement for tfap2a independent of Hox regulation. Early melanophores do not develop in low mutants, and we propose that this results in part from a loss of kit function, leading to defects in migration, as well as kit-independent defects in melanophore specification. Iridophores are also reduced in low, in contrast to xanthophores, revealing a role for tfap2a in the development of pigment subpopulations. We propose a model of tfap2a function in the neural crest in which there are independent functions for tfap2a in specification of subpopulations of pigment cells and segmental patterning of the pharyngeal skeleton through the regulation of Hox genes.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping