The small GTPase Rab23 has a well-known role as an antagonist of sonic hedgehog signalling during embryonic development. However, recent evidence suggests that it also has an embryogenesis-independent ciliary function, although the exact nature of this role is unknown. Here (p. ), Bor Luen Tang and Yi Shan Lim shed light on the role of Rab23 in cilia by demonstrating that it acts in ciliary protein trafficking. They found that Rab23 and a constitutively active Rab23 Q68L mutant both localised to the primary cilium in NIH3T3, hTERT-retinal pigment epithelial (hTERT-RPE1) and CRL1927 cells, when they are overexpressed. Knockdown (KD) of Rab23 did not cause any significant ciliary defects, indicating that Rab23 does not have a crucial function in ciliogenesis. However, in both NIH3T3 and in hTERT-RPE1 cells, Rab23 overexpression increased the ciliary localisation of the kinesin-2 family motor Kif17, whereas Rab23 KD decreased the ciliary localisation of Kif17. Furthermore, the localisation of Kif17 to cilia was rescued when the authors re-expressed Rab23 in Rab23 KD cells, confirming that the observed effect is Rab23 specific. Finally, the authors determined that Rab23 forms a complex with Kif17 and its putative ciliary import adaptor importin β2 in a manner that strongly depends on GTP-binding. Taken together, these data indicate that Rab23 functions in the ciliary trafficking of Kif17 through a mechanism that is most likely to involve facilitating the interaction between Kif17 and importin β2.
