The movement of ciliary membrane proteins is directed by transient interactions with intraflagellar transport (IFT) trains. The green alga Chlamydomonas has adapted this process for gliding motility, using retrograde IFT motors to move adhesive glycoproteins in the flagella membrane. Ca²⁺ signalling contributes directly to the gliding process, although uncertainty remains over the mechanism through which it acts. Here, we show that flagella Ca²⁺ elevations initiate the movement of paused retrograde IFT trains, which accumulate at the distal end of adherent flagella, but do not influence other IFT processes. On highly adherent surfaces, flagella exhibit high-frequency Ca²⁺ elevations that prevent the accumulation of paused retrograde IFT trains. Flagella Ca²⁺ elevations disrupt the IFT-dependent movement of microspheres along the flagella membrane, suggesting that Ca²⁺ acts by directly disrupting an interaction between retrograde IFT trains and flagella membrane glycoproteins. By regulating the extent to which glycoproteins on the flagella surface interact with IFT motor proteins on the axoneme, this signalling mechanism allows precise control of traction force and gliding motility in adherent flagella.

睫状膜蛋白的运动是通过与鞭毛内运输（IFT）序列的短暂相互作用来指导的。绿藻衣藻使用逆行IFT马达使鞭毛膜中的黏附糖蛋白移动，从而使该过程适应了滑翔运动。Ca ²⁺信号直接影响滑​​行过程，尽管其作用机理尚不确定。在这里，我们显示鞭毛Ca ²⁺升高启动了暂停的逆行IFT列车的运动，该运动积累在附着的鞭毛的远端，但不影响其他IFT过程。在高度附着的表面上，鞭毛表现出高频的Ca ²⁺防止暂停的逆行IFT列车积聚的高度。鞭毛Ca ^2+的升高破坏了微球沿着鞭毛膜的IFT依赖性运动，表明Ca ²⁺通过直接破坏逆行IFT序列和鞭毛膜糖蛋白之间的相互作用而起作用。通过调节鞭毛表面糖蛋白与轴突上IFT马达蛋白相互作用的程度，这种信号传导机制可以精确控制附着鞭毛的牵引力和滑动运动。