Nkx5-1 is a transcription factor expressed early during the inner ear development, and it is necessary for the formation of semicircular canals. Evolution of the Nkx5 family of genes, and functional properties of the Nkx5-1 protein, were investigated in the presented work. Five previously identified medaka Nkx5 genes were characterized by obtaining their full genomic and coding sequences, and by analysis of their expression patterns. Phylogenetic analysis of Nkx5 family members revealed the existence of four paralogous groups of Nkx5 genes in the vertebrate genome, and only one in invertebrate species. In medaka genome representatives of all four groups are present (in contrast to other vertebrates, were some Nkx5 genes have been lost or still await discovery), and the Nkx5-1 gene is represented by two paralogs. This situation is in line with recent hypotheses postulating genome duplications in the evolutionary history of vertebrates. The obtained data led me to propose a model of evolutionary history of this ancient group of genes. In the zebrafish FGF8 mutant, acerebellar (ace), ear placodes and vesicles are strongly diminished, and ear expression of several transcription factors is downregulated in comparison to wild type. I isolated the zebrafish Nkx5-1 cDNA, and studied its expression in wild type and ace embryos. It appeared that zfNkx5-1 is strongly downregulated in the ace otic placodes and vesicles. Subsequently I studied effects of the ectopic FGF source on expression of Nkx5-1 and other ear transcription factors, using chicken as a model system. The experiment proved that additional FGF source can activate expression of Nkx5-1, SOHo and Pax2 genes, while slightly downregulating Dlx5 expression. Additionally, FGF2 sources were able to induce ectopic ear structures. In chicken embryos FGF8 is transiently expressed in the anterior part of the placode, at time and place suggesting that FGF8 might regulate Nkx5-1 expression. In the mouse and chicken ear Dlx5 pattern of expression is very similar to Nkx5-1 pattern; the Dlx5 KO mice show strong semicircular canals malformations, very much alike Nkx5-1 -/- mice. I studied the expression of Nkx5-1 in the Dlx5 mutant ears and vice versa, and expression of both genes appeared to be mutually independent; this result suggests that Nkx5-1 and Dlx5 do not regulate each other's expression. One of the candidate genes for the Nkx5-1 target is BMP4, since in the Nkx5-1 -/- ear it is downregulated. To find out whether Nkx5-1 is able to induce BMP4 expression, I injected zfNkx5-1 mRNA into the two cell medaka embryos. Indeed, the BMP4 domain is much stronger at the injected site, however, additional effects of the Nkx5-1 injections demand a further investigation.