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

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.

Pubmed ID: 18056639 RIS Download

Mesh terms: Animals | Animals, Genetically Modified | Biological Transport | Body Patterning | Cell Line | Centrosome | Cilia | Gene Expression Regulation, Developmental | Gene Expression Regulation, Enzymologic | Humans | Microtubules | Phosphotransferases (Alcohol Group Acceptor) | Protozoan Proteins | Zebrafish | Zebrafish Proteins

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Associated grants

  • Agency: NCRR NIH HHS, Id: 1S10RR15682
  • Agency: NCI NIH HHS, Id: CA68485
  • Agency: NIDDK NIH HHS, Id: DK20593
  • Agency: NIGMS NIH HHS, Id: GM51912
  • Agency: NINDS NIH HHS, Id: NS46668

ZFIN (Data, Gene Expression)

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