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Functional and biophysical analyses of the class XIV Toxoplasma gondii Myosin D
Authors:ANGELIKA HERM-GÖTZ  FRÊDÊRIC DELBAC  STEFAN WEISS  MIKLOS NYITRAI  ROLF STRATMANN  STANISLAS TOMAVO  L. DAVID SIBLEY  MICHAEL A. GEEVES  DOMINIQUE SOLDATI
Affiliation:(1) Hygieneinstitut, Universitätsklinikum Heidelberg, Im Neuenheimer Feld 324, D-69120 Heidelberg, Germany;(2) Zentrum für Molekulare Biologie, Universität Heidelberg, Im Neuenheimer Feld 282, D-69120 Heidelberg, Germany;(3) Laboratoire Biologie des Protistes, UMR CNRS 6023, Université Blaise Pascal, 24 av. des Landais, 63177 Aubière cedex, France;(4) Department of Biosciences, University of Kent, CT2 7NJ Canterbury, UK;(5) Laboratoire de Chimie Biologique CNRS UMR 8576, Bâtiment C9 Université des Sciences et Technologies de Lille, 59655 Villeneuve d’Ascq, France;(6) Department of Molecular Microbiology, Washington University School of Medicine, St. Louis, MO 63110, USA;(7) Present address: Department of Biophysics, University of Pécs, Pécs, Hungary;(8) Heidelberger Institut für Pflanzenwissenschaften, Universität Heidelberg, Im Neuenheimer Feld 360, D-69120 Heidelberg, Germany;(9) Present address: Department of Microbiology and Molecular Medicine, Faculty of Medicine, University of Geneva CMU, 1 Rue Michel-Servet, 1211 Geneva 4, Switzerland
Abstract:Summary The obligate intracellular parasite Toxoplasma gondii uses gliding motility to migrate across the biological barriers of the host and to invade cells. This unique form of locomotion requires an intact actin cytoskeleton and involves at least one motor protein (TgMyoA) that belongs to the class XIV of the myosin superfamily. TgMyoA is anchored in the inner membrane complex and is essential for the gliding motion, host cell invasion and egress of T. gondii tachyzoites. TgMyoD is the smallest T. gondii myosin and is structurally very closely related to TgMyoA. We show here that TgMyoD exhibits similar transient kinetic properties as the fast single-headed TgMyoA. To determine if TgMyoD also contributes to parasite gliding motility, the TgMyoD gene was disrupted by double homologous recombination. In contrast to TgMyoA, TgMyoD gene is dispensable for tachyzoite propagation and motility. Parasites lacking TgMyoD glide normally and their virulence is not compromised in mice. The fact that TgMyoD is predominantly expressed in bradyzoites explains the absence of a phenotype observed with myodko in tachyzoites and does not exclude a role of this motor in gliding that would be restricted to the cyst forming but nevertheless motile stage of the parasite.Both authors contributed equally to the work.
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