The Role of CEP164B in Trypanosoma brucei: Implications for Flagellum Biogenesis and Cell Cycle Regulation

Abstract

Trypanosoma brucei is the causative agent of Human African Trypanosomiasis (HAT) or African Sleeping Sickness. The protozoan kinetoplast relies on precise cell cycle regulation and flagellum biogenesis for survival and pathogenicity. The transition fibre protein CEP164B has been implicated in flagellar assembly, yet its specific role in trypanosome cell division remains underexplored. This study investigates the impact of CEP164B depletion on cell morphology, flagellum formation and cell cycle progression in T.brucei using RNA interference (RNAi). Fluorescence microscopy and quantitative analysis revealed that CEP164B interference significantly reduced flagellum length, the emergence of abnormal cell populations, including 0K1N cells (no kinetoplast, one nucleus), and defects in kinetoplast segregation. Statistical analyses confirmed significant shifts in cell populations, with a decline in 1K1N cells and an increase in multinucleated and mutant forms. The observed phenotypes suggest that CEP164B plays a crucial role in maintaining transition fibre integrity, basal body positioning, and coordinated organelle division. These findings highlight CEP164B as a potential therapeutic target for disrupting trypanosome proliferation