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Fgf3 and Fgf10 are required for mouse otic placode induction.
Tracy J Wright1, Suzanne L Mansour
1Department of Human Genetics, University of Utah, Salt Lake City, UT 84112-5330, USA.
Summary
Fibroblast Growth Factor (FGF) signals from the hindbrain and mesenchyme are crucial for inner ear development. Simultaneous loss of Fgf3 and Fgf10 prevents otic vesicle formation, highlighting their essential role in placode induction.
Area of Science:
- Developmental Biology
- Genetics
- Otic Development
Background:
- The inner ear, responsible for hearing and balance, develops from an ectodermal placode near the hindbrain.
- Previous studies indicated Fibroblast Growth Factor (FGF) signaling involvement, with Fgf3 affecting later stages of otic vesicle formation.
Purpose of the Study:
- To investigate the role of FGF signaling, specifically Fgf3 and Fgf10, in early otic placode induction and development.
- To determine the origins of FGF signals directing otic placode formation.
Main Methods:
- Analysis of mouse embryos with combined Fgf3 and Fgf10 gene knockouts.
- Examination of otic marker gene expression patterns in mutant embryos.
- Assessment of cell proliferation and survival in double mutant embryos.
Main Results:
- Embryos lacking both Fgf3 and Fgf10 failed to form otic vesicles.
- Aberrant expression of otic marker genes was observed in double mutants.
- FGF signals appear to act directly on the ectoderm, as hindbrain gene expression remained normal.
- Cell proliferation and survival were not significantly impacted, suggesting a role in gene regulation.
Conclusions:
- FGF signals from both the hindbrain and mesenchyme are essential for otic placode induction.
- The primary role of FGF signaling in otic induction is to establish correct gene expression patterns in the prospective placode.
- A quantitative requirement for FGF signaling in otic vesicle formation was suggested by intermediate phenotypes in triple mutant embryos.