Jan 15, 2014

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

BioRxiv : the Preprint Server for Biology
Saskia EgarterMarkus Meissner

Abstract

Apicomplexan parasites are thought to actively invade the host cell by gliding motility. This movement is powered by the parasite 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 identified, mutant parasites remain invasive and do not show a block of gliding motility, demonstrating that other mechanisms must be in place to enable the parasite to move and invade the host cell. A novel model for parasite gliding motility and invasion is presented based on hydrodynamic forces generated in the cytosol of the parasite that are converted into motility.

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Mentioned in this Paper

Glideosome-associated protein 45, Plasmodium falciparum
Study
MLC1 protein, human
MLC1
MyoA protein, Aspergillus nidulans
Microneme
Actos
Cell Motility
Actins
Motor protein

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