ABSTRACT FGF3 has been involved in the development of the inner ear in a number of species including mouse, chicken and Xenopus. Initial experiments using antisense oligonucleotides in explants of chicken embryos indicated a role for FGF3 for proper formation of the otic vesicle (Represa et al., 1991). However, mice carrying a mutant FGF3 allele exhibited normal formation of the otic vesicle and only showed defects during later differentiation of the inner ear (Mansour et al., 1993). Implantation of beads incubated with FGF3 into Xenopus embryos led to the formation of ectopic vesicles (Lombardo et al., 1998). To further resolve the functions of FGF3 during inner ear development we recently performed gainof-function experiments in chicken embryos by ectopically expressing FGF3 via a Herpes simplex-derived viral vector (Vendrell et al., 2000). Embryos infected by the virus developed ectopic otic vesicles confirming the involvement of FGF3 during formation of the otic vesicle in avians. To further clarify the role of FGF3 during inner ear development in vertebrates, we have now addressed its potential function in zebrafish.

To analyse the function of FGF3 for otic development we chose a loss-of-function approach using antisense morpholino oligomers designed to block translation of fgf3 transcripts. Morpholinos have been shown to cause developmental defects that closely mimic phenotypes caused by null mutations in the same genes (Nasevicius and Ekker, 2000). In the light of the contrasting evidence for the involvement of FGF3 during formation of the otic vesicle we were particularly interested to analyse potential defects during this process. We therefore monitored formation of the otic vesicle in injected and control embryos using a Pax2 antibody which stains the otic placode and vesicle during zebrafish development (Püschel et al., 1992).