PUBLICATION
dackel acts in the ectoderm of the zebrafish pectoral fin bud to maintain AER signaling
- Authors
- Grandel, H., Draper, B.W., and Schulte-Merker, S.
- ID
- ZDB-PUB-001101-7
- Date
- 2000
- Source
- Development (Cambridge, England) 127(19): 4169-4178 (Journal)
- Registered Authors
- Draper, Bruce, Grandel, Heiner, Schulte-Merker, Stefan
- Keywords
- pectoral fin; limb; dorsoventral axis; zebrafish; dackel
- MeSH Terms
-
- Animals
- Ectoderm*
- Embryonic Induction*
- Epidermis/embryology
- Extremities
- Fibroblast Growth Factor 4
- Fibroblast Growth Factor 8
- Fibroblast Growth Factors/metabolism
- Genes, Homeobox
- Hedgehog Proteins
- Homeodomain Proteins/metabolism
- Limb Buds/embryology
- Morphogenesis
- Mutation
- Proteins/metabolism*
- Proto-Oncogene Proteins/metabolism
- Tissue Transplantation
- Trans-Activators*
- Transcription Factors*
- Zebrafish/embryology
- Zebrafish Proteins*
- PubMed
- 10976049 Full text @ Development
Citation
Grandel, H., Draper, B.W., and Schulte-Merker, S. (2000) dackel acts in the ectoderm of the zebrafish pectoral fin bud to maintain AER signaling. Development (Cambridge, England). 127(19):4169-4178.
Abstract
Classical embryological studies have implied the existence of an apical ectodermal maintenance factor (AEMF) that sustains signaling from the apical ectodermal ridge (AER) during vertebrate limb development. Recent evidence suggests that AEMF activity is composed of different signals involving both a sonic hedgehog (Shh) signal and a fibroblast growth factor 10 (Fgf10) signal from the mesenchyme. In this study we show that the product of the dackel (dak) gene is one of the components that acts in the epidermis of the zebrafish pectoral fin bud to maintain signaling from the apical fold, which is homologous to the AER of tetrapods. dak acts synergistically with Shh to induce fgf4 and fgf8 expression but independently of Shh in promoting apical fold morphogenesis. The failure of dak mutant fin buds to progress from the initial fin induction phase to the autonomous outgrowth phase causes loss of both AER and Shh activity, and subsequently results in a proximodistal truncation of the fin, similar to the result obtained by ridge ablation experiments in the chicken. Further analysis of the dak mutant phenotype indicates that the activity of the transcription factor engrailed 1 (En1) in the ventral non-ridge ectoderm also depends on a maintenance signal probably provided by the ridge. This result uncovers a new interaction between the AER and the dorsoventral organizer in the zebrafish pectoral fin bud.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping