| First Author | Chaya T | Year | 2014 |
| Journal | EMBO J | Volume | 33 |
| Issue | 11 | Pages | 1227-42 |
| PubMed ID | 24797473 | Mgi Jnum | J:211665 |
| Mgi Id | MGI:5575827 | Doi | 10.1002/embj.201488175 |
| Citation | Chaya T, et al. (2014) ICK is essential for cell type-specific ciliogenesis and the regulation of ciliary transport. EMBO J 33(11):1227-42 |
| abstractText | 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. |
