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Biophysical Characterization of Flagellar Motor Functions
Published on: January 18, 2017
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Flagellar cAMP signaling controls trypanosome progression through host tissues
Sebastian Shaw1,2, Stephanie F DeMarco3, Ruth Rehmann1
1Institute of Cell Biology, University of Bern, Baltzerstrasse 4, CH-3012, Bern, Switzerland.
Nature Communications
|February 20, 2019
Summary
Trypanosoma brucei parasites need flagellar phosphodiesterase PDEB1 to move through tsetse fly guts. Without PDEB1, parasites get stuck, preventing transmission and disease spread.
Area of Science:
- Parasitology
- Cell Biology
- Insect Vector Biology
Background:
- Trypanosoma brucei causes African trypanosomiasis in mammals.
- Transmission occurs via tsetse flies, involving complex parasite development within the insect.
- Flagellar phosphodiesterase PDEB1 (PDEB1) is known to be essential for social motility in vitro.
Purpose of the Study:
- To investigate the role of PDEB1 in the development and transmission of Trypanosoma brucei within the tsetse fly vector.
- To understand the mechanisms by which parasites navigate the insect midgut environment.
Main Methods:
- Generation of PDEB1 knockout Trypanosoma brucei parasites.
- Infection of tsetse flies with wild-type and knockout parasites.
- Live confocal microscopy of fluorescent parasites within dual-labelled insect tissues.
Main Results:
- PDEB1 knockout parasites showed subtle motility defects, similar to bacterial chemotaxis mutants.
- PDEB1 is crucial for parasites to traverse the peritrophic matrix in the tsetse fly midgut.
- Parasites lacking PDEB1 were retained in the midgut lumen and could not progress in their life cycle.
Conclusions:
- The peritrophic matrix represents a significant barrier to parasite migration within the tsetse fly.
- The flagellar cAMP signaling pathway, mediated by PDEB1, is essential for overcoming this barrier.
- Parasite migration and progression through the tsetse fly life cycle depend on active traversal mechanisms, potentially involving chemotaxis.
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