Molecular dissection of host cell invasion by the apicomplexans: the glideosome.
Gliding motility is an essential and fascinating apicomplexan-typical adaptation to an intracellular lifestyle. Apicomplexan parasites rely on gliding motility for their migration across biological barriers and for host cell invasion and egress. This unusual substratedependent mode of locomotion involves the concerted action of secretory adhesins, a myosin motor, factors regulating actin dynamics and proteases. During invasion, complexes of soluble and transmembrane micronemes proteins (MICs) and rhoptry neck proteins (RONs) are discharged to the apical pole of the parasite, some protein acts as adhesins and bind to host cell receptors whereas others are involved in the moving junction formation. These complexes redistribute towards the posterior pole of the parasite via a physical connection to the parasite actomyosin system and are eventually released from the parasite surface by the action of parasite proteases.
Soldati-Favre
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Department of Microbiology and Molecular Medicine, CMU, University of Geneva, 1, rue Michel-Servet, 1211 Geneva 4, Switzerland. dominique.soldati-favre@medecine.unige.ch
D000205:Actomyosin / Q000737:chemistry / Q000502:physiology; D000818:Animals; D016782:Apicomplexa / Q000166:cytology / Q000502:physiology* / Q000648:ultrastructure; D002448:Cell Adhesion / Q000502:physiology*; D002465:Cell Movement / Q000502:physiology*; D003599:Cytoskeleton; D006790:Host-Parasite Interactions; D006801:Humans; D008565:Membrane Proteins / Q000737:chemistry / Q000502:physiology; D020409:Molecular Motor Proteins / Q000502:physiology*; D011528:Protozoan Infections / Q000469:parasitology*; D015800:Protozoan Proteins / Q000737:chemistry / Q000502:physiology*
D008565:Membrane Proteins; D020409:Molecular Motor Proteins; D015800:Protozoan Proteins; D000205:Actomyosin