Zebrafish ift57, ift88, and ift172 intraflagellar transport mutants disrupt cilia but do not affect hedgehog signaling
Article first published online: 10 JUN 2009
Copyright © 2009 Wiley-Liss, Inc.
Volume 238, Issue 7, pages 1744–1759, July 2009
How to Cite
Lunt, S. C., Haynes, T. and Perkins, B. D. (2009), Zebrafish ift57, ift88, and ift172 intraflagellar transport mutants disrupt cilia but do not affect hedgehog signaling. Dev. Dyn., 238: 1744–1759. doi: 10.1002/dvdy.21999
- Issue published online: 10 JUN 2009
- Article first published online: 10 JUN 2009
- Manuscript Accepted: 29 APR 2009
- NIH. Grant Number: EY017037
Cilia formation requires intraflagellar transport (IFT) proteins. Recent studies indicate that mammalian Hedgehog (Hh) signaling requires cilia. It is unclear, however, if the requirement for cilia and IFT proteins in Hh signaling represents a general rule for all vertebrates. Here we examine zebrafish ift57, ift88, and ift172 mutants and morphants for defects in Hh signaling. Although ift57 and ift88 mutants and morphants contained residual maternal protein, the cilia were disrupted. In contrast to previous genetic studies in mouse, mutations in zebrafish IFT genes did not affect the expression of Hh target genes in the neural tube and forebrain and had no quantitative effect on Hh target gene expression. Zebrafish IFT mutants also exhibited no dramatic changes in the craniofacial skeleton, somite formation, or motor neuron patterning. Thus, our data indicate the requirement for cilia in the Hh signal transduction pathway may not represent a universal mechanism in vertebrates. Developmental Dynamics 238:1744–1759, 2009. © 2009 Wiley-Liss, Inc.