Role of Toxoplasma gondii Myosin A in Powering Parasite Gliding and Host Cell Invasion

• DOI: 10.1126/science.1074553
• Publication Date: 2002-10-24T21:03:20Z
• Authors: Markus Meissner; Dirk Schlüter; Dominique Soldati
• Keywords: 0301 basic medicine; Calcium/metabolism; Movement; Virulence Factors/physiology; Genetic Vectors; Toxoplasma/genetics/growth & development/pathogenicity/physiology; Protozoan Proteins; Transfection; Exocytosis; Tetracycline/pharmacology; Cell Line; Nonmuscle Myosin Type IIA/genetics/physiology; Mice; 03 medical and health sciences; Toxoplasmosis, Animal/parasitology; info:eu-repo/classification/ddc/616; Organelles/metabolism; Animals; Humans; Transgenes; Trans-Activators/metabolism; Calcimycin; Cells, Cultured; ddc:616; Organelles; Calcimycin/pharmacology; Virulence; Nonmuscle Myosin Type IIA; Tetracycline; Protozoan Proteins/genetics/physiology; Toxoplasmosis, Animal; Trans-Activators; Calcium; Toxoplasma

Obligate intracellular apicomplexan parasites rely on gliding motion powered by their actomyosin system to disperse throughout tissues and to penetrate host cells. Toxoplasma gondii myosin A has been implicated in this process, but direct proof has been lacking. We designed a genetic screen to generate a tetracycline-inducible transactivator system in T. gondii . The MyoA gene was disrupted in the presence of a second regulatable copy of MyoA . Conditional removal of this myosin caused severe impairment in host cell invasion and parasite spreading in cultured cells, and unambiguously established the pathogenic function of this motor in an animal model.