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Background  Primary cilia are essential for Hedgehog (Hh) signal transduction in vertebrates. Although the core components of the Hh pathway are highly conserved, the dependency on cilia in Hh signaling is considered to be lower in fish than in mice, suggesting the presence of species-specific mechanisms for Hh signal transduction.    Results  To precisely understand the role of cilia in Hh signaling in fish and explore the evolution of Hh signaling, we have generated a maternal-zygotic medaka ( Oryzias latipes ) mutant that lacks  cytoplasmic dynein heavy chain 2  ( dhc2 ; MZ dhc2 ), a component required for retrograde intraflagellar transport. We found that MZ dhc2  exhibited the shortened cilia and partial defects in Hh signaling, although the Hh defects were milder than zebrafish mutants which completely lack cilia. This result suggests that Hh activity in fish depends on the length of cilium. However, the activity of Hh signaling in MZ dhc2  appeared to be higher than that in mouse  Dnchc2  mutants, suggesting a lower requirement for cilia in Hh signaling in fish. We confirmed that Ptch1 receptor is exclusively localized on the cilium in fish as in mammals. Subsequent analyses revealed that Fused, an essential mediator for Hh signaling in  Drosophila  and fish but not in mammals, augments the activity of Hh signaling in fish as a transcriptional target of Hh signaling.    Conclusions  Ciliary requirement for Hh signaling in fish is lower than that in mammals, possibly due to  fused -mediated positive feedback in Hh signaling. The finding of this fish-specific augmentation provides a novel insight into the evolution of Hh signaling.    Electronic supplementary material  The online version of this article (doi:10.1186/s12861-015-0057-x) contains supplementary material, which is available to authorized users.

The medaka dhc2 mutant reveals conserved and distinct mechanisms of Hedgehog signaling in teleosts