EMD-6749
Representative tomogram for the Trypanosoma brucei zoid cell with flagellar wave
EMD-6749
Tomography
Map released: 13/06/2018
Last modified: 26/12/2018
Sample Organism:
Trypanosoma brucei
Sample: Trypanosoma brucei cell
Deposition Authors: Sun SY, Kaelber JT, Chen M, Shi J, Schmid MF, Chiu W, He CY
Sample: Trypanosoma brucei cell
Deposition Authors: Sun SY, Kaelber JT, Chen M, Shi J, Schmid MF, Chiu W, He CY
Flagellum couples cell shape to motility inTrypanosoma brucei.
Sun SY,
Kaelber JT
,
Chen M,
Dong X,
Nematbakhsh Y,
Shi J,
Dougherty M,
Lim CT,
Schmid MF
,
Chiu W,
He CY
(2018) PNAS , 115 , E5916 - E5925
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(2018) PNAS , 115 , E5916 - E5925
Abstract:
In the unicellular parasite Trypanosoma 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 that T. brucei can 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 engineered T. brucei to 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 for T. brucei to disseminate in its host through size-limiting barriers.
In the unicellular parasite Trypanosoma 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 that T. brucei can 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 engineered T. brucei to 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 for T. brucei to disseminate in its host through size-limiting barriers.