The planar cell polarity protein Fuzzy (Fuz) promotes ciliogenesis by delivering intraflagellar transport (IFT) proteins to the basal bodies of primary cilia, Brooks and Wallingford report.
Fuz is required for cilia assembly in frogs and mice, but how it supports ciliogenesis is unknown. The protein has no obvious functional domains, though bioinformatic analyses point to a possible role in vesicle trafficking. Brooks and Wallingford found that multiciliated frog cells lacking Fuz failed to transport several proteins to the distal ends of their cilia, suggesting that Fuz might regulate the movements of IFT particles, protein complexes that shuttle cargo back and forth along the cilium's microtubules.
The researchers imaged the dynamics of IFT complexes in multiciliated cells and found that the particles stalled in the absence of Fuz. The arrested particles lacked IFT43, a component of the IFT-A complex that recycles proteins back from cilia tips. IFT particles are assembled at the basal bodies of primary cilia, but IFT43 wasn't recruited to these structures in Fuz-deficient cells. The particles lacking IFT43 can probably move to cilia tips but fail to complete the return journey, eventually blocking traffic in both directions and disrupting cilia assembly.
It remains to be seen how Fuz brings IFT43 to basal bodies. Senior author John Wallingford now wants to investigate exactly where in the cell Fuz operates and to identify binding partners that aid its trafficking function.
