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Plasmodium motility: actin not actin' like actin.
Herwig Schüler1, Kai Matuschewski
1Max Delbrück Center for Molecular Medicine, 13125 Berlin, Germany. schueler@mdc-berlin.de
Trends in Parasitology
|February 28, 2006
Summary
Parasitic motility, like that of Plasmodium and Toxoplasma, may rely on transient, short actin filament scaffolds. Myosin interaction with these scaffolds propels parasites forward.
Area of Science:
- Parasitology
- Cell Biology
- Biophysics
Background:
- Apicomplexan parasites (e.g., Plasmodium, Toxoplasma) exhibit actomyosin-dependent motility.
- This motility occurs despite a lack of easily detectable, long actin polymers within the parasites.
Purpose of the Study:
- To investigate the mechanism of apicomplexan motility.
- To propose a model for how short actin filaments facilitate parasite movement.
Main Methods:
- Analysis of actin polymer length from harvested parasites.
- Formation and analysis of actin polymers from purified recombinant parasite actin proteins.
Main Results:
- Parasite-derived and recombinant actin polymers are exceptionally short, measuring approximately 100 nm.
- These short actin filaments are proposed to form transient scaffolds.
Conclusions:
- Parasite motility is likely driven by the transient formation of short actin filament scaffolds.
- Myosin interaction with these scaffolds pulls transmembrane receptors, enabling parasite locomotion.