PUBLICATION
Zebrafish fgf24 functions with fgf8 to promote posterior mesodermal development
- Authors
- Draper, B.W., Stock, D.W., and Kimmel, C.B.
- ID
- ZDB-PUB-030826-13
- Date
- 2003
- Source
- Development (Cambridge, England) 130(19): 4639-4654 (Journal)
- Registered Authors
- Draper, Bruce, Kimmel, Charles B., Stock, David W.
- Keywords
- none
- MeSH Terms
-
- Gene Expression Regulation, Developmental
- T-Box Domain Proteins/metabolism
- Gastrula/cytology
- Gastrula/physiology
- Phylogeny
- Mice
- Animals
- Fetal Proteins
- Zebrafish/anatomy & histology
- Zebrafish/embryology*
- Zebrafish/physiology
- Sequence Alignment
- Amino Acid Sequence
- Humans
- Oligonucleotides, Antisense/metabolism
- Mesoderm/physiology*
- Ligands
- Zebrafish Proteins/chemistry
- Zebrafish Proteins/classification
- Zebrafish Proteins/genetics
- Zebrafish Proteins/metabolism*
- Fibroblast Growth Factors/chemistry
- Fibroblast Growth Factors/genetics
- Fibroblast Growth Factors/metabolism*
- Molecular Sequence Data
- Enhancer Elements, Genetic
- Signal Transduction/physiology*
- Fibroblast Growth Factor 8
- PubMed
- 12925590 Full text @ Development
Citation
Draper, B.W., Stock, D.W., and Kimmel, C.B. (2003) Zebrafish fgf24 functions with fgf8 to promote posterior mesodermal development. Development (Cambridge, England). 130(19):4639-4654.
Abstract
Fibroblast growth factor (Fgf) signaling plays an important role during development of posterior mesoderm in vertebrate embryos. Blocking Fgf signaling by expressing a dominant-negative Fgf receptor inhibits posterior mesoderm development. In mice, Fgf8 appears to be the principal ligand required for mesodermal development, as mouse Fgf8 mutants do not form mesoderm. In zebrafish, Fgf8 is encoded by the acerebellar locus, and, similar to its mouse otholog, is expressed in early mesodermal precursors during gastrulation. However, zebrafish fgf8 mutants have only mild defects in posterior mesodermal development, suggesting that it is not the only Fgf ligand involved in the development of this tissue. We report here the identification of an fgf8-related gene in zebrafish, fgf24, that is co-expressed with fgf8 in mesodermal precursors during gastrulation. Using morpholino-based gene inactivation, we have analyzed the function of fgf24 during development. We found that inhibiting fgf24 function alone has no affect on the formation of posterior mesoderm. Conversely, inhibiting fgf24 function in embryos mutant for fgf8 blocks the formation of most posterior mesoderm. Thus, fgf8 and fgf24 are together required to promote posterior mesodermal development. We provide both phenotypic and genetic evidence that these Fgf signaling components interact with no tail and spadetail, two zebrafish T-box transcription factors that are required for the development of all posterior mesoderm. Last, we show that fgf24 is expressed in early fin bud mesenchyme and that inhibiting fgf24 function results in viable fish that lack pectoral fins.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping