TY  - JOUR
A1  - Schuster, Sarah
A1  - Krüger, Timothy
A1  - Subota, Ines
A1  - Thusek, Sina
A1  - Rotureau, Brice
A1  - Beilhack, Andreas
A1  - Engstler, Markus
T1  - Developmental adaptations of trypanosome motility to the tsetse fly host environments unravel a multifaceted in vivo microswimmer system
JF  - eLife
N2  - The highly motile and versatile protozoan pathogen Trypanosoma brucei undergoes a complex life cycle in the tsetse fly. Here we introduce the host insect as an expedient model environment for microswimmer research, as it allows examination of microbial motion within a diversified, secluded and yet microscopically tractable space. During their week-long journey through the different microenvironments of the fly´s interior organs, the incessantly swimming trypanosomes cross various barriers and confined surroundings, with concurrently occurring major changes of parasite cell architecture. Multicolour light sheet fluorescence microscopy provided information about tsetse tissue topology with unprecedented resolution and allowed the first 3D analysis of the infection process. High-speed fluorescence microscopy illuminated the versatile behaviour of trypanosome developmental stages, ranging from solitary motion and near-wall swimming to collective motility in synchronised swarms and in confinement. We correlate the microenvironments and trypanosome morphologies to high-speed motility data, which paves the way for cross-disciplinary microswimmer research in a naturally evolved environment.
KW  - none
KW  - tsetse fly
KW  - Trypanosoma
KW  - biophysics
KW  - microswimmer
KW  - sleeping sickness
KW  - structural biology
Y1  - 2017
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-158662
VL  - 6
ER  - 
TY  - JOUR
A1  - Zimmermann, Henriette
A1  - Subota, Ines
A1  - Batram, Christopher
A1  - Kramer, Susanne
A1  - Janzen, Christian J.
A1  - Jones, Nicola G.
A1  - Engstler, Markus
T1  - A quorum sensing-independent path to stumpy development in Trypanosoma brucei
JF  - PLoS Pathogens
N2  - For persistent infections of the mammalian host, African trypanosomes limit their population size by quorum sensing of the parasite-excreted stumpy induction factor (SIF), which induces development to the tsetse-infective stumpy stage. We found that besides this cell density-dependent mechanism, there exists a second path to the stumpy stage that is linked to antigenic variation, the main instrument of parasite virulence. The expression of a second variant surface glycoprotein (VSG) leads to transcriptional attenuation of the VSG expression site (ES) and immediate development to tsetse fly infective stumpy parasites. This path is independent of SIF and solely controlled by the transcriptional status of the ES. In pleomorphic trypanosomes varying degrees of ES-attenuation result in phenotypic plasticity. While full ES-attenuation causes irreversible stumpy development, milder attenuation may open a time window for rescuing an unsuccessful antigenic switch, a scenario that so far has not been considered as important for parasite survival.
KW  - Trypanosoma
KW  - hyperexpression techniques
KW  - parasitic cell cycles
KW  - cloning
KW  - cell cycle and cell division
KW  - cell differentiation
KW  - tetracyclines
KW  - parasitic diseases
Y1  - 2017
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-158230
VL  - 13
IS  - 4
ER  -