PUBLICATION
Fibroblast Growth Factor Receptors Function Redundantly During Zebrafish Embryonic Development
- Authors
- Leerberg, D.M., Hopton, R.E., Draper, B.W.
- ID
- ZDB-PUB-190609-4
- Date
- 2019
- Source
- Genetics 212(4): 1301-1319 (Journal)
- Registered Authors
- Draper, Bruce, Leerberg, Dena M.
- Keywords
- Fibroblast growth factor signaling, midbrain-hindbrain boundary, neurocranium, pectoral fin, posterior mesoderm, viscerocranium
- MeSH Terms
-
- Animals
- Brain/embryology
- Brain/metabolism*
- Embryonic Development*
- Fibroblast Growth Factors/genetics*
- Fibroblast Growth Factors/metabolism
- Mesoderm/embryology
- Mesoderm/metabolism*
- Receptors, Fibroblast Growth Factor/genetics*
- Receptors, Fibroblast Growth Factor/metabolism
- Zebrafish
- Zebrafish Proteins/genetics*
- Zebrafish Proteins/metabolism
- PubMed
- 31175226 Full text @ Genetics
Citation
Leerberg, D.M., Hopton, R.E., Draper, B.W. (2019) Fibroblast Growth Factor Receptors Function Redundantly During Zebrafish Embryonic Development. Genetics. 212(4):1301-1319.
Abstract
Fibroblast growth factor (Fgf) signaling regulates many processes during development. In most cases, one tissue layer secretes an Fgf ligand that binds and activates an Fgf receptor (Fgfr) expressed by a neighboring tissue. Although studies have identified the roles of specific Fgf ligands during development, less is known about the requirements for the receptors. We have generated null mutations in each of the five fgfr genes in zebrafish. Considering the diverse requirements for Fgf signaling throughout development and that null mutations in the mouse Fgfr1 and Fgfr2 genes are embryonic lethal, it was surprising that all zebrafish homozygous mutants are viable and fertile, with no discernable embryonic defect. Instead, we find that multiple receptors are involved in coordinating most Fgf-dependent developmental processes. For example, mutations in the ligand fgf8a cause loss of the midbrain-hindbrain boundary, whereas in the fgfr mutants, this phenotype is only seen in embryos that are triple mutant for fgfr1a;fgfr1b;fgfr2, but not in any single or double mutant combinations. We show that this apparent fgfr redundancy is also seen during the development of several other tissues, including posterior mesoderm, pectoral fins, viscerocranium, and neurocranium. These data are an essential step towards defining the specific Fgfrs that function with particular Fgf ligands to regulate important developmental processes in zebrafish.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping