2. Academic Validation
  3. ICK is essential for cell type-specific ciliogenesis and the regulation of ciliary transport

ICK is essential for cell type-specific ciliogenesis and the regulation of ciliary transport

  • EMBO J. 2014 Jun 2;33(11):1227-42. doi: 10.1002/embj.201488175.
Taro Chaya 1,  Yoshihiro Omori 2,  Ryusuke Kuwahara 3,  Takahisa Furukawa 4
Affiliations

Affiliations

  • 1 Laboratory for Molecular and Developmental Biology, Institute for Protein Research Osaka University, Suita Osaka, Japan JST CREST, Suita Osaka, Japan Department of Developmental Biology, Osaka Bioscience Institute, Suita Osaka, Japan Kyoto University Graduate School of Medicine, Sakyo-ku Kyoto, Japan.
  • 2 Laboratory for Molecular and Developmental Biology, Institute for Protein Research Osaka University, Suita Osaka, Japan JST CREST, Suita Osaka, Japan Department of Developmental Biology, Osaka Bioscience Institute, Suita Osaka, Japan JST PRESTO, Suita Osaka, Japan.
  • 3 Research Center for Ultrahigh Voltage Electron Microscopy Osaka University, Ibaraki Osaka, Japan.
  • 4 Laboratory for Molecular and Developmental Biology, Institute for Protein Research Osaka University, Suita Osaka, Japan JST CREST, Suita Osaka, Japan Department of Developmental Biology, Osaka Bioscience Institute, Suita Osaka, Japan [email protected].
PMID: 24797473 DOI: 10.1002/embj.201488175
Abstract

Cilia and flagella are formed and maintained by intraflagellar transport (IFT) and play important roles in sensing and moving across species. At the distal tip of the cilia/flagella, IFT complexes turn around to switch from anterograde to retrograde transport; however, the underlying regulatory mechanism is unclear. Here, we identified ICK localization at the tip of cilia as a regulator of ciliary transport. In ICK-deficient mice, we found ciliary defects in neuronal progenitor cells with Hedgehog signal defects. ICK-deficient cells formed cilia with mislocalized Hedgehog signaling components. Loss of ICK caused the accumulation of IFT-A, IFT-B, and BBSome components at the ciliary tips. In contrast, overexpression of ICK induced the strong accumulation of IFT-B, but not IFT-A or BBSome components at ciliary tips. In addition, ICK directly phosphorylated Kif3a, while inhibition of this Kif3a phosphorylation affected ciliary formation. Our results suggest that ICK is a Kif3a kinase and essential for proper ciliogenesis in development by regulating ciliary transport at the tip of cilia.

Keywords

ciliary transport; ciliogenesis; kinase; kinesin.

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