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PLoS One. 2014 Mar 14;9(3):e91819. doi: 10.1371/journal.pone.0091819. eCollection 2014.

The toxoplasma Acto-MyoA motor complex is important but not essential for gliding motility and host cell invasion.

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Wellcome Trust Centre for Molecular Parasitology, Institute of Infection, Immunity & Inflammation, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, United Kingdom.
Nuffield Department of Clinical Laboratory Science, Oxford University, Oxford, United Kingdom.
Institut Cochin, University of Paris Descartes, INSERM U-1016, CNRS UMR-8104, Paris, France.
Department of Neurobiology, Physiology, and Behavior and Department of Mathematics, University of California Davis, Davis, California, United States of America.


Apicomplexan parasites are thought to actively invade the host cell by gliding motility. This movement is powered by the parasite's own actomyosin system, and depends on the regulated polymerisation and depolymerisation of actin to generate the force for gliding and host cell penetration. Recent studies demonstrated that Toxoplasma gondii can invade the host cell in the absence of several core components of the invasion machinery, such as the motor protein myosin A (MyoA), the microneme proteins MIC2 and AMA1 and actin, indicating the presence of alternative invasion mechanisms. Here the roles of MyoA, MLC1, GAP45 and Act1, core components of the gliding machinery, are re-dissected in detail. Although important roles of these components for gliding motility and host cell invasion are verified, mutant parasites remain invasive and do not show a block of gliding motility, suggesting that other mechanisms must be in place to enable the parasite to move and invade the host cell. A novel, hypothetical model for parasite gliding motility and invasion is presented based on osmotic forces generated in the cytosol of the parasite that are converted into motility.

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