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A role for the inositol kinase Ipk1 in ciliary beating and length maintenance.


Sarmah| Winfrey| Olson| Appel| Wente B| VP| GE| B| SRBhaskarjyoti| Virginia P| Gary E| Bruce| Susan R . Proceedings of the National Academy of Sciences of the United States of America. 2007 12 11; 104(50). 19843-8


Cilia project from cells as membranous extensions, with microtubule structural cores assembling from basal bodies by intraflagellar transport (IFT). Here, we report a ciliary role for the inositol 1,3,4,5,6-pentakisphosphate 2-kinase (Ipk1) that generates inositol hexakisphosphate. In zebrafish embryos, reducing Ipk1 levels inhibited ciliary beating in Kupffer’s vesicle and decreased ciliary length in the spinal canal, pronephric ducts, and Kupffer’s vesicle. Electron microscopy showed that ciliary axonemal structures were not grossly altered. However, coincident knockdown of Ipk1 and IFT88 or IFT57 had synergistic perturbations. With GFP-Ipk1 enriched in centrosomes and basal bodies, we propose that Ipk1 plays a previously uncharacterized role in ciliary function.

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