Abstract
In the unicellular parasiteTrypanosoma brucei,the causative agent of human African sleeping sickness, complex swimming behavior is driven by a flagellum laterally attached to the long and slender cell body. Using microfluidic assays, we demonstrated thatT. bruceican penetrate through an orifice smaller than its maximum diameter. Efficient motility and penetration depend on active flagellar beating. To understand how active beating of the flagellum affects the cell body, we genetically engineeredT. bruceito produce anucleate cytoplasts (zoids and minis) with different flagellar attachment configurations and different swimming behaviors. We used cryo-electron tomography (cryo-ET) to visualize zoids and minis vitrified in different motility states. We showed that flagellar wave patterns reflective of their motility states are coupled to cytoskeleton deformation. Based on these observations, we propose a mechanism for how flagellum beating can deform the cell body via a flexible connection between the flagellar axoneme and the cell body. This mechanism may be critical forT. bruceito disseminate in its host through size-limiting barriers.
Funder
HHS | NIH | National Institute of General Medical Sciences
Ministry of Education - Singapore
Publisher
Proceedings of the National Academy of Sciences
Cited by
30 articles.
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