Volume 15, Number 3, September 2008Xth European Multicolloquium of Parasitology (EMOP-10, Paris, August 24-28, 2008)
|Page(s)||197 - 205|
|Published online||15 September 2008|
Xth EMOP, August 2008
Molecular dissection of host cell invasion by the Apicomplexans: the glideosome
Department of Microbiology and Molecular Medicine, CMU, University of Geneva, 1, rue Michel-Servet, 1211 Geneva 4, Switzerland
* Tel.: + 41 22 379 5672 – Fax: + 41 22 379 5702. E-mail: firstname.lastname@example.org
Gliding motility is an essential and fascinating apicomplexantypical 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 substrate-dependent 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.
Key words: Toxoplasma gondii / Plasmodium falciparum / Apicomplexa / adhesin / microneme / actin / myosin / proteases
© PRINCEPS Editions, Paris, 2008, transferred to Société Française de Parasitologie
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