PUBLICATION
The roles of the FGF signal in zebrafish embryos analyzed using constitutive activation and dominant-negative suppression of different FGF receptors
- Authors
- Ota, S., Tonou-Fujimori, N., and Yamasu, K.
- ID
- ZDB-PUB-081121-21
- Date
- 2009
- Source
- Mechanisms of Development 126(1-2): 1-17 (Journal)
- Registered Authors
- Ota, Satoshi, Yamasu, Kyo
- Keywords
- none
- MeSH Terms
-
- Embryo, Nonmammalian/embryology*
- Embryo, Nonmammalian/metabolism*
- Gene Expression Regulation, Developmental
- Zebrafish/embryology*
- Zebrafish/genetics
- Zebrafish/metabolism*
- Fibroblast Growth Factors/metabolism*
- Animals
- Signal Transduction*
- RNA, Messenger/genetics
- Solubility
- Body Patterning
- Ligands
- Receptors, Fibroblast Growth Factor/deficiency
- Receptors, Fibroblast Growth Factor/genetics
- Receptors, Fibroblast Growth Factor/metabolism*
- PubMed
- 19015027 Full text @ Mech. Dev.
Citation
Ota, S., Tonou-Fujimori, N., and Yamasu, K. (2009) The roles of the FGF signal in zebrafish embryos analyzed using constitutive activation and dominant-negative suppression of different FGF receptors. Mechanisms of Development. 126(1-2):1-17.
Abstract
The roles of the FGF family growth factors and their receptors (FGFRs) in zebrafish embryos were examined using variously modified versions of the four FGFR genes (fgfr1-4). Constitutively active forms of all of the examined FGFRs (ca-FGFRs) caused dorsalization, brain caudalization, and secondary axis formation, indicating that the main FGF signal transduction downstream of the receptor is highly similar among FGFRs. All of the membrane-bound type of dominant-negative FGFRs (mdn-FGFRs) derived from the four fgfr genes, which interfere with endogenous FGFRs, produced posterior truncation, as previously reported in both Xenopus and zebrafish. mdn-FGFR3c had the strongest effects on embryos, progressively disrupting the posterior structure as the dose increased. At the highest dose, only the forebrain was formed. At lower doses, mdn-FGFR3c mainly suppressed the paraxial mesoderm. The co-injection of mRNA for different mdn-FGFRs and FGFs resulted in diverse suppression spectra of the respective FGFRs against FGFs. Only mdn-FGFR3c severely suppressed all of the FGFs examined. We also examined the effects of the secretory type of dominant-negative FGFRs (sdn-FGFRs), which are released from cells and trap FGF ligands. Only sdn-FGFR3c resulted in the characteristic effect of selectively disrupting the isthmic development, as well as the tailbud. The co-injection of the mRNA for sdn-FGFRs and FGFs suggested that sdn-FGFR3c inhibits FGFs of the FGF8 subfamily, which is consistent with its specific effects on development. We discuss the implications of our findings obtained in the present study.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping