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ICK is essential for cell type‐specific ciliogenesis and the regulation of ciliary transport
Author(s) -
Chaya Taro,
Omori Yoshihiro,
Kuwahara Ryusuke,
Furukawa Takahisa
Publication year - 2014
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1002/embj.201488175
Subject(s) - cilium , ciliogenesis , intraflagellar transport , microbiology and biotechnology , biology , flagellum , smoothened , ciliopathy , hedgehog , anatomy , signal transduction , phenotype , biochemistry , gene
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 BBS ome components at the ciliary tips. In contrast, overexpression of ICK induced the strong accumulation of IFT ‐ B , but not IFT ‐ A or BBS ome components at ciliary tips. In addition, ICK directly phosphorylated K if3a, while inhibition of this K if3a phosphorylation affected ciliary formation. Our results suggest that ICK is a K if3a kinase and essential for proper ciliogenesis in development by regulating ciliary transport at the tip of cilia.