FAZ assembly in bloodstream form Trypanosoma brucei requires kinesin KIN-E

Trypanosoma brucei, the causative agent of African sleeping sickness, uses its flagellum for movement, cell division, and signaling. The flagellum is anchored to the cell body membrane via the flagellum attachment zone (FAZ), a complex of proteins, filaments, and microtubules that spans two membranes with elements on both flagellum and cell body sides. How FAZ components are carried into place to form this complex is poorly understood. Here, we show that the trypanosome-specific kinesin KIN-E is required for building the FAZ in bloodstream-form parasites. KIN-E is localized along the flagellum with a concentration at its distal tip. Depletion of KIN-E by RNAi rapidly inhibits flagellum attachment and leads to cell death. A detailed analysis reveals that KIN-E depletion phenotypes include failure in cytokinesis completion, kinetoplast DNA missegregation, and transport vesicle accumulation. Together with previously published results in procyclic form parasites, these data suggest KIN-E plays a critical role in FAZ assembly in T. brucei.

Automated summary

This study reveals that the trypanosome-specific kinesin KIN-E is crucial for the assembly of the flagellum attachment zone (FAZ) in bloodstream-form Trypanosoma brucei. Depletion of KIN-E inhibits flagellum attachment and leads to cell death, with phenotypes including failure in cytokinesis completion, kinetoplast DNA missegregation, and transport vesicle accumulation.