Induction of inner ear fate by FGF3

TLDR

Loss‑of‑function studies in avians and mammals have yielded conflicting evidence on whether fibroblast growth factor 3 (FGF3) acts as a secreted factor that induces and morphogenetically shapes the vertebrate inner ear. The study seeks to re‑evaluate the role of FGF3 in avian inner ear development. This was done by applying a novel gene‑transfer technique to chicken embryos. Ectopic FGF3 expression generates ectopic placodes that express otic markers, form vesicles with a developing inner ear gene‑expression pattern, alter normal inner ear formation, and shows that a single gene can induce inner ear fate, revealing a broad competence of surface ectoderm to form sensory placodes in higher vertebrates.

Abstract

ABSTRACT Loss-of-function experiments in avians and mammals have provided conflicting results on the capacity of fibroblast growth factor 3 (FGF3) to act as a secreted growth factor responsible for induction and morphogenesis of the vertebrate inner ear. Using a novel technique for gene transfer into chicken embryos, we have readdressed the role of FGF3 during inner ear development in avians. We find that ectopic expression of FGF3 results in the formation of ectopic placodes which express otic marker genes. The ectopically induced placodes form vesicles which show the characteristic gene expression pattern of a developing inner ear. Ectopic expression of FGF3 also influences the formation of the normal orthotopic inner ear, whereas another member of the FGF family, FGF2, shows no effects on inner ear induction. These results demonstrate that a single gene can induce inner ear fate and reveal an unexpectedly widespread competence of the surface ectoderm to form sensory placodes in higher vertebrates.