The length of cilia is robustly regulated . Previous data suggest that cells possess a sensing system to control ciliary length [2-5]. However, the details of the mechanism are currently not known [6, 7]. Such a system requires a mechanism that responds to ciliary length, and consequently, disruption of that response system should alter ciliary length . The assembly rate of cilium mediated by intraflagellar transport (IFT) gradually decreases as the cilium elongates and eventually is balanced by the constant rate of disassembly, at which point cilium elongation stops [8, 9]. Because the rate of IFT entry into the cilium also decreases as the cilium elongates , regulation of IFT entry could provide the mechanism for length control. Previously, we showed that phosphorylation of the FLA8/KIF3B subunit of the anterograde kinesin-II IFT motor blocks IFT entry and flagellar assembly in Chlamydomonas . Here, we show in Chlamydomonas that cellular signaling in response to alteration of flagellar length regulates phosphorylation of FLA8/KIF3B, which restricts IFT entry and, thus, flagellar assembly to control flagellar length. Cellular levels of phosphorylated FLA8 (pFLA8) are tightly linked to flagellar length: FLA8 phosphorylation is reduced in cells with short flagella and elevated in cells with long flagella. Depletion of the phosphatases CrPP1 and CrPP6 increases the level of cellular pFLA8, leading to short flagella due to decreased IFT entry. The results demonstrate that ciliary length control is achieved by a cellular sensing system that controls IFT entry through phosphorylation of the anterograde IFT motor.
Keywords: Chlamydomonas; IFT; cilia; ciliary length control; flagella; intraflagellar transport; kinesin-2; protein phosphorylation.
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