Figure 7.

Model of IFTA-1 function as a component of retrograde IFT. Presented is an extension of previous models by Snow et al. (2004) and Ou et al. (2005a), where two kinesin-2 motors were shown to drive anterograde IFT (heterotrimeric kinesin-II, drawn in brown; and homodimeric OSM-3-kinesin, drawn in blue), and BBS-7 and BBS-8 proteins were found to stabilize the association of IFT-A and IFT-B subcomplexes. (A) Loss of IFTA-1 function causes a ciliary accumulation of IFT machinery components, including IFT-B subcomplexes and the IFT-A subcomplex protein (CHE-11), indicating that IFTA-1 function is not required for entry of IFT machinery assemblies into cilia via anterograde IFT but that it is required for recycling of the IFT machinery back to the base of cilia via retrograde IFT. Defective retrograde IFT results in a partial loss of the singlet-microtubule-derived distal segment. (B) The IFT-A subcomplex gene mutant che-11 closely phenocopies the retrograde IFT defects of ifta-1 mutants. In addition, CHE-11 function is required for the ciliary localization of IFTA-1 protein. (C) Together, the data presented in A and B indicate that in wild-type C. elegans sensory cilia, IFTA-1 is closely associated with IFT-A subcomplexes and functions within the retrograde arm of the IFT process.