期刊
EMBO JOURNAL
卷 33, 期 11, 页码 1227-1242出版社
WILEY-BLACKWELL
DOI: 10.1002/embj.201488175
关键词
ciliary transport; ciliogenesis; kinase; kinesin
资金
- CREST from Japan Science and Technology Agency
- PRESTO from Japan Science and Technology Agency
- Ministry of Education, Culture, Sports, Science and Technology of Japan
- Takeda Science Foundation
- Uehara Memorial Foundation
- Research Foundation for Opto-Science and Technology
- Mitsubishi Foundation
- Suzuken Memorial Foundation
- Japan Foundation for Applied Enzymology
- 'Nanotechnology Platform' of the Ministry of Education, Culture, Sports, Science and Technology (MEXT), Japan [12024046]
- Grants-in-Aid for Scientific Research [25113519] Funding Source: KAKEN
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.
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