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      Conservation of a Gliding Motility and Cell Invasion Machinery in Apicomplexan Parasites

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          Abstract

          Most Apicomplexan parasites, including the human pathogens Plasmodium, Toxoplasma, and Cryptosporidium, actively invade host cells and display gliding motility, both actions powered by parasite microfilaments. In Plasmodium sporozoites, thrombospondin-related anonymous protein (TRAP), a member of a group of Apicomplexan transmembrane proteins that have common adhesion domains, is necessary for gliding motility and infection of the vertebrate host. Here, we provide genetic evidence that TRAP is directly involved in a capping process that drives both sporozoite gliding and cell invasion. We also demonstrate that TRAP-related proteins in other Apicomplexa fulfill the same function and that their cytoplasmic tails interact with homologous partners in the respective parasite. Therefore, a mechanism of surface redistribution of TRAP-related proteins driving gliding locomotion and cell invasion is conserved among Apicomplexan parasites.

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          TRAP is necessary for gliding motility and infectivity of plasmodium sporozoites.

          Ali A Sultan, Vandana Thathy, Ute Frevert … (1997)
          Many protozoans of the phylum Apicomplexa are invasive parasites that exhibit a substrate-dependent gliding motility. Plasmodium (malaria) sporozoites, the stage of the parasite that invades the salivary glands of the mosquito vector and the liver of the vertebrate host, express a surface protein called thrombospondin-related anonymous protein (TRAP) that has homologs in other Apicomplexa. By gene targeting in a rodent Plasmodium, we demonstrate that TRAP is critical for sporozoite infection of the mosquito salivary glands and the rat liver, and is essential for sporozoite gliding motility in vitro. This suggests that in Plasmodium sporozoites, and likely in other Apicomplexa, gliding locomotion and cell invasion have a common molecular basis.
          Article 0 comments Cited 166 times – based on 0 reviews     Review now
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            Toxoplasma invasion of mammalian cells is powered by the actin cytoskeleton of the parasite.

            J M Dobrowolski, L D Sibley (1996)
            Toxoplasma gondii is an obligate intracellular parasite that invades a wide range of vertebrate host cells. We demonstrate that invasion is critically dependent on actin filaments in the parasite, but not the host cell. Invasion into cytochalasin D (CD)-resistant host cells was blocked by CD, while parasite mutants invaded wild-type host cells in the presence of drug. CD resistance in Toxoplasma was mediated by a point mutation in the single-copy actin gene ACT1. Transfection of the mutant act1 allele into wild-type Toxoplasma conferred motility and invasion in the presence of CD. We conclude that host cell invasion by Toxoplasma, and likely by related Apicomplexans, is actively powered by an actin-based contractile system in the parasite.
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              Sequential protein secretion from three distinct organelles of Toxoplasma gondii accompanies invasion of human fibroblasts.

              V B Carruthers, L D Sibley (1997)
              Invasion of vertebrate cells by the protozoan Toxoplasma gondii is accompanied by regulated protein secretion from three distinct parasite organelles called micronemes, rhoptries, and dense granules. We have compared the kinetics of secretion from these different compartments during host cell invasion using immunofluorescence, immunoelectron microscopy, and quantitative immunoassays. Binding to the host cell triggered apical release of the micronemal protein MIC2 at the tight attachment zone that forms between the parasite and the host cell. In a second step, invagination of the host cell plasma membrane was initiated by discharge of the rhoptry protein ROP1 to form a nascent parasitophorous vacuole (PV). ROP1 was fully discharged into the vacuole by the time invasion was complete. In contrast to these very rapid early events, release of the dense granule markers GRA1 and NTPase was delayed until after the parasite was fully within the PV, eventually peaking at 20 min post-invasion. The sequential triggering of secretion from different organelles implies that their release is governed by separate signals and that their contents mediate distinct phases of intracellular parasitism.
              Article 0 comments Cited 148 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                :
                Department of Pathology, Division of Immunology, New York University School of Medicine, 550 First Avenue, New York, NY 10016.(212) 263-8179(212) 263-7870
                Journal
                Journal ID (nlm-ta): J Cell Biol
                Title: The Journal of Cell Biology
                Publisher: The Rockefeller University Press
                ISSN (Print): 0021-9525
                ISSN (Electronic): 1540-8140
                Publication date (Print): 29 November 1999
                Volume: 147
                Issue: 5
                Pages: 937-944
                Affiliations
                [a ]Department of Pathology, Kaplan Cancer Center
                [b ]Department of Medical and Molecular Parasitology, New York University School of Medicine, New York, New York 10016
                [c ]Case Western Reserve University School of Medicine, Cleveland, Ohio 44106
                Article
                Publisher ID: 9909141
                DOI: 10.1083/jcb.147.5.937
                PMC ID: 2169348
                PubMed ID: 10579715
                SO-VID: 9b9a2741-8f7d-4a13-83be-374887f9abae
                Copyright © © 1999 The Rockefeller University Press
                History
                Date received : 30 September 1999
                Date revision requested : 18 October 1999
                Date accepted : 18 October 1999
                Categories
                Subject: Brief Report

                ScienceOpen disciplines: Cell biology
                Keywords: gliding motility,cell invasion,apicomplexan parasites,thrombospondin-related anonymous protein,micronemal protein 2
                Data availability:
                ScienceOpen disciplines: Cell biology
                Keywords: gliding motility, cell invasion, apicomplexan parasites, thrombospondin-related anonymous protein, micronemal protein 2

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