PUBLICATION

Dampened Hedgehog signaling but normal Wnt signaling in zebrafish without cilia

Authors
Huang, P., and Schier, A.F.
ID
ZDB-PUB-090828-14
Date
2009
Source
Development (Cambridge, England)   136(18): 3089-3098 (Journal)
Registered Authors
Huang, Peng, Schier, Alexander
Keywords
Cilia, Hedgehog signaling, Wnt signaling, Gli, Spinal cord, Somite, Zebrafish
MeSH Terms
  • Animals
  • Animals, Genetically Modified
  • Body Patterning
  • Cilia/metabolism*
  • Epistasis, Genetic
  • Hedgehog Proteins/genetics
  • Hedgehog Proteins/metabolism*
  • In Situ Hybridization
  • Oligonucleotides, Antisense
  • Oncogene Proteins/genetics
  • Oncogene Proteins/metabolism
  • Signal Transduction/physiology*
  • Trans-Activators/genetics
  • Trans-Activators/metabolism
  • Wnt Proteins/genetics
  • Wnt Proteins/metabolism*
  • Zebrafish*/anatomy & histology
  • Zebrafish*/embryology
  • Zebrafish*/metabolism
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism*
PubMed
19700616 Full text @ Development
Abstract
Cilia have been implicated in Hedgehog (Hh) and Wnt signaling in mouse but not in Drosophila. To determine whether the role of cilia is conserved in zebrafish, we generated maternal-zygotic (MZ) oval (ovl; ift88) mutants that lack all cilia. MZovl mutants display normal canonical and non-canonical Wnt signaling but show defects in Hh signaling. As in mouse, zebrafish cilia are required to mediate the activities of Hh, Ptc, Smo and PKA. However, in contrast to mouse Ift88 mutants, which show a dramatic reduction in Hh signaling, zebrafish MZovl mutants display dampened, but expanded, Hh pathway activity. This activity is largely due to gli1, the expression of which is fully dependent on Hh signaling in mouse but not in zebrafish. These results reveal a conserved requirement for cilia in transducing the activity of upstream regulators of Hh signaling but distinct phenotypic effects due to differential regulation and differing roles of transcriptional mediators.
Genes / Markers
Figures
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Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping