CKA is required for adult motor coordination. (A) Effect of depletion of CKA in late larval brains on viability and adult motor coordination. Expression of transgenes in late larval stages was controlled by feeding RU-486. Loss of neuronal CKA late in development has a minor effect on viability but results in a pronounced uncoordinated phenotype. This phenotype is rescued by BFP-CKA but not BFP-CKA^ΔPP2A expression. (B) A model for the function of a STRIPAK complex in axonal transport. CKA functions as a scaffold protein, binding core STRIPAK components Mob4, Strip, and the structural subunit PP2A (A), as well as kinases. Strip binds directly to the P150 subunit of the dynactin complex (Sakuma et al., 2014). Dynactin is a regulatory complex of dynein, and the dynein/dynactin association is necessary for retrograde transport. CKA binds directly to Atg8a, a protein that localizes to the membrane of autophagosomes. As a core STRIPAK component, CKA mediates attachment of autophagosomes to dynein/dynactin transport machinery. The STRIPAK complex also tethers PP2A and kinases that may coregulate the dynein-mediated transport of a subset of organelles.