Mesodermal Fgf10b cooperates with other Fgfs during induction of otic and epibranchial placodes in zebrafish
- Maulding, K., Padanad, M.S., Dong, J., Riley, B.B.
- Developmental dynamics : an official publication of the American Association of Anatomists 243(10): 1275-85 (Journal)
- Registered Authors
- Padanad, Mahesh, Riley, Bruce
- cranial placodes, epibranchial ganglia, otic vesicle, pax2a, phox2a, sox3
- MeSH Terms
- Animals, Genetically Modified
- Body Patterning/genetics
- Branchial Region/embryology*
- Branchial Region/metabolism
- Embryo, Nonmammalian
- Embryonic Induction/genetics*
- Fibroblast Growth Factor 10/physiology
- Fibroblast Growth Factor 3/physiology*
- Fibroblast Growth Factors/physiology*
- Zebrafish Proteins/physiology*
- 24677486 Full text @ Dev. Dyn.
Maulding, K., Padanad, M.S., Dong, J., Riley, B.B. (2014) Mesodermal Fgf10b cooperates with other Fgfs during induction of otic and epibranchial placodes in zebrafish. Developmental dynamics : an official publication of the American Association of Anatomists. 243(10):1275-85.
Background Vertebrate otic and epibranchial placodes develop in close proximity in response to localized fibroblast growth factor (Fgf) signaling. Although less is known about epibranchial induction, the process of otic induction in highly conserved, with important roles for Fgf3 and Fgf8 reported in all species examined. Fgf10 is also critical for otic induction in mouse, but the only zebrafish ortholog examined to date, fgf10a, is not expressed early enough to play such a role. A second zebrafish ortholog, fgf10b, has not been previously examined.
Results We find that zebrafish fgf10b is expressed at tailbud stage in paraxial cephalic mesoderm beneath prospective epibranchial tissue, lateral to the developing otic placode. Knockdown of fgf10b does not affect initial otic induction but impairs subsequent accumulation of otic cells. Formation of epibranchial placodes and ganglia are also moderately impaired. Combinatorial disruption of fgf10b and fgf3 exacerbates the deficiency of otic cells and eliminates epibranchial induction entirely. Disruption of fgf10b and fgf24 also strongly reduces, but does not eliminate, epibranchial induction.
Conclusions fgf10b participates in a late phase of otic induction and, in combination with fgf3, is especially critical for epibranchial induction.
Genes / Markers
Mutation and Transgenics
Human Disease / Model Data
Sequence Targeting Reagents
Engineered Foreign Genes
Errata and Notes