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© The Rockefeller University Press, 0021-9525/2001/11/613 $5.00
The Journal of Cell Biology, Volume 155, Number 4, November 12, 2001 613-624

Toxoplasma gondii myosins B/C

Frédéric Delbac^1,2, Astrid Sänger¹, Eva M. Neuhaus³, Rolf Stratmann¹, James W. Ajioka⁴, Catherine Toursel⁵, Angelika Herm-Götz¹, Stanislas Tomavo⁵, Thierry Soldati³ and Dominique Soldati¹

¹ Zentrum für Molekulare Biologie, Universität Heidelberg, D-69120 Heidelberg, Germany
² Laboratoire de Biologie des Protistes, Centre National de la Recherche Scientifique (CNRS), UMR 6023, Université Blaise Pascal, 63177 Aubière, France
³ Department of Molecular Cell Research, Max Planck Institute for Medical Research, D-69120 Heidelberg, Germany
⁴ Department of Pathology, University of Cambridge, Cambridge CB2 1QP, United Kingdom
⁵ UMR CNRS 8576 Université des Sciences et Technologies de Lille, France

Address correspondence to Dr. Dominique Soldati, Department of Biological Sciences, Imperial College of Science, Technology, and Medicine, Imperial College Road, London SW7 2AZ, United Kingdom. Tel.: (44) 207-594-5342. Fax: (44) 207-584-2056. E-mail: d.soldati{at}ic.ac.uk

In apicomplexan parasites, actin-disrupting drugs and the inhibitor of myosin heavy chain ATPase, 2,3-butanedione monoxime, have been shown to interfere with host cell invasion by inhibiting parasite gliding motility. We report here that the actomyosin system of Toxoplasma gondii also contributes to the process of cell division by ensuring accurate budding of daughter cells. T. gondii myosins B and C are encoded by alternatively spliced mRNAs and differ only in their COOH-terminal tails. MyoB and MyoC showed distinct subcellular localizations and dissimilar solubilities, which were conferred by their tails. MyoC is the first marker selectively concentrated at the anterior and posterior polar rings of the inner membrane complex, structures that play a key role in cell shape integrity during daughter cell biogenesis. When transiently expressed, MyoB, MyoC, as well as the common motor domain lacking the tail did not distribute evenly between daughter cells, suggesting some impairment in proper segregation. Stable overexpression of MyoB caused a significant defect in parasite cell division, leading to the formation of extensive residual bodies, a substantial delay in replication, and loss of acute virulence in mice. Altogether, these observations suggest that MyoB/C products play a role in proper daughter cell budding and separation.

Key Words: Apicomplexa; unconventional myosin XIV; localization; Toxoplasma gondii; cell division

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