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Background  The inner ear arises from a specialized set of cells, the otic placode, that forms at the lateral edge of the neural plate adjacent to the hindbrain. Previous studies indicated that fibroblast growth factors (Fgfs) are required for otic induction; in zebrafish, loss of both Fgf3 and Fgf8 results in total ablation of otic tissue. Furthermore, gain-of-function studies suggested that Fgf signaling is not only necessary but also sufficient for otic induction, although the amount of induced ectopic otic tissue reported after misexpression of  fgf3  or  fgf8  varies among different studies. We previously suggested that Foxi1 and Dlx3b may provide competence to form the ear because loss of both  foxi 1 and  dlx3b  results in ablation of all otic tissue even in the presence of a fully functional Fgf signaling pathway.    Results  Using a transgenic line that allows us to misexpress  fgf8  under the control of the zebrafish temperature-inducible  hsp70  promoter, we readdressed the role of Fgf signaling and otic competence during placode induction. We find that misexpression of  fgf8  fails to induce formation of ectopic otic vesicles outside of the endogenous ear field and has different consequences depending upon the developmental stage. Overexpression of  fgf8  from 1-cell to midgastrula stages leads to formation of no or small otic vesicles, respectively. Overexpression of  fgf8  at these stages never leads to ectopic expression of  foxi1  or  dlx3b , contrary to previous studies that indicated that  foxi1  is activated by Fgf signaling. Consistent with our results we find that pharmacological inhibition of Fgf signaling has no effect on  foxi1  or  dlx3b  expression, but instead, Bmp signaling activates  foxi1 , directly and  dlx3b , indirectly. In contrast to early activation of  fgf8 ,  fgf8  overexpression at the end of gastrulation, when otic induction begins, leads to much larger otic vesicles. We further show that application of a low dose of retinoic acid that does not perturb patterning of the anterior neural plate leads to expansion of  foxi1  and to a massive Fgf-dependent otic induction.    Conclusion  These results provide further support for the hypothesis that Foxi1 and Dlx3b provide competence for cells to respond to Fgf and form an otic placode.

Fgf-dependent otic induction requires competence provided by Foxi1 and Dlx3b