The role of the cytoskeleton in host cell invasion by Toxoplasma gondii.
The protozoan parasite Toxoplasma gondii provides a model system for studying invasion by intracellular parasites belonging to the phylum Apicomplexa. Taking advantage of the versatility of T. gondii for genetic and cell biological studies, we have shown that parasite motility and cell invasion are powered by an actin-myosin based motor in the parasite. Unlike bacterial cell uptake, parasite invasion does not involve significant alterations in the host cell cytoskeleton. Instead, invasion is an active process of penetration into the host cell by the parasite. The force for cell penetration is provided by a unique form of substrate-dependent motility termed gliding. Gliding motility is characterized by the rearward capping of surface membrane proteins that propels the parasite forward in a helical spiral. Both actin and myosin are localized beneath the plasma membrane in the parasite where they presumably combine to produce the force necessary for motility. During cell invasion, the rearward capping of cell surface receptors envelopes the parasite in a unique vacuole derived from the host cell plasma membrane. This system offers insights into force generation and motility in a simple organism that is also an important human pathogen.
Dobrowolski
J
J
Department of Molecular Microbiology, Washington University School of Medicine, St. Louis, MO 63110, USA.
Sibley
L D
LD
D000818:Animals; D016782:Apicomplexa / Q000502:physiology; D003599:Cytoskeleton / Q000469:parasitology*; D006790:Host-Parasite Interactions; D006801:Humans; D008565:Membrane Proteins / Q000502:physiology; D009068:Movement; D010587:Phagocytosis; D015800:Protozoan Proteins / Q000502:physiology; D014122:Toxoplasma / Q000469:parasitology / Q000502:physiology*; D014123:Toxoplasmosis / Q000469:parasitology* / Q000503:physiopathology
D008565:Membrane Proteins; D015800:Protozoan Proteins