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      Gliding motility powers invasion and egress in Apicomplexa

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      Nature Reviews Microbiology
      Springer Nature

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          Abstract

          Apicomplexa include important human pathogens and possess a unique cellular machinery that promotes gliding motility and is called the glideosome. In this Review, Soldati-Favre and colleagues discuss the principles that govern gliding motility, the characterization of the molecular machinery that comprises the glideosome, and its impact on parasite invasion and egress from infected cells.

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          Most cited references134

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          Molecular motors.

          Life implies movement. Most forms of movement in the living world are powered by tiny protein machines known as molecular motors. Among the best known are motors that use sophisticated intramolecular amplification mechanisms to take nanometre steps along protein tracks in the cytoplasm. These motors transport a wide variety of cargo, power cell locomotion, drive cell division and, when combined in large ensembles, allow organisms to move. Motor defects can lead to severe diseases or may even be lethal. Basic principles of motor design and mechanism have now been derived, and an understanding of their complex cellular roles is emerging.
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            TRAP is necessary for gliding motility and infectivity of plasmodium sporozoites.

            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.
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              Toxoplasma invasion of mammalian cells is powered by the actin cytoskeleton of the parasite.

              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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                Author and article information

                Journal
                Nature Reviews Microbiology
                Nat Rev Micro
                Springer Nature
                1740-1526
                1740-1534
                September 4 2017
                September 4 2017
                :
                :
                Article
                10.1038/nrmicro.2017.86
                28867819
                3728af2e-3e34-4bca-ae75-159206a2470e
                © 2017
                History

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