Intraflagellar transport (IFT) is required for ciliary assembly and maintenance. While disruption of IFT may trigger ciliary disassembly, we show here that IFT mediated transport of a CDK-like kinase ensures proper ciliary disassembly. Mutations in flagellar shortening 2 (FLS2), encoding a CDK-like kinase, lead to retardation of cilia resorption and delay of cell cycle progression. Stimulation for ciliary disassembly induces gradual dephosphorylation of FLS2 accompanied with gradual inactivation. Loss of FLS2 or its kinase activity induces early onset of kinesin13 phosphorylation in cilia. FLS2 is predominantly localized in the cell body, however, it is transported to cilia upon induction of ciliary disassembly. FLS2 directly interacts with IFT70 and loss of this interaction inhibits its ciliary transport, leading to dysregulation of kinesin13 phosphorylation and retardation of ciliary disassembly. Thus, this work demonstrates that IFT plays active roles in controlling proper ciliary disassembly by transporting a protein kinase to cilia to regulate a microtubule depolymerizer.

睫状体组装和维护需要鞭毛内运输（IFT）。虽然IFT的破坏可能会触发睫状体的拆卸，但我们在这里表明IFT介导的CDK样激酶的转运可确保适当的睫状体的拆卸。鞭毛缩短2（FLS2），编码CDK样激酶，导致纤毛吸收延迟和细胞周期进程延迟。刺激睫状体分解可诱导FLS2逐渐脱磷酸并伴随逐渐失活。FLS2或其激酶活性的丧失会引起纤毛中的驱动蛋白13磷酸化的早期发作。FLS2主要位于细胞体内，但是在诱导睫状体分解时将其转运至纤毛。FLS2直接与IFT70相互作用，这种相互作用的丧失抑制了其纤毛运输，从而导致驱动蛋白13磷酸化失调和纤毛分解阻滞。因此，这项工作表明，IFT通过将蛋白激酶转运至纤毛以调节微管解聚剂，在控制适当的睫状体分解中起着积极作用。