An orphan kinesin controls trypanosome morphology transitions by targeting FLAM3 to the flagellum

摘要: Trypanosoma brucei undergoes life cycle form transitions from trypomastigotes to epimastigotes in the insect vector by re-positioning mitochondrial genome and re-locating flagellum flagellum-associated cytoskeletal structures. The mechanism underlying these dramatic morphology remains poorly understood. Here we report regulatory role of orphan kinesin KIN-E controlling trypanosome transitions. localizes is enriched at flagellar tip, this localization depends on C-terminal m-calpain domain III-like domains. Depletion trypomastigote T. causes major changes a gradual increase level EP procyclin, generating epimastigote-like cells. Mechanistically, through its importin α-like domain, targets FLAM3, protein involved transitions, promote elongation attachment zone positioning structure, thereby maintaining cell morphology. Our findings suggest that trypanosomes require KIN-E-mediated transport FLAM3 flagellum.