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  • The EMBO Journal (2001) 20, 330 - 339
  • doi:10.1093/emboj/20.3.330

A plastid segregation defect in the protozoan parasite Toxoplasma gondii

Cynthia Y. He1, Michael K. Shaw1, Charles H. Pletcher2, Boris Striepen3, Lewis G. Tilney1 and David S. Roos1

  1. Department of Biology, 305 Goddard Laboratories, University of Pennsylvania, Philadelphia, PA 19104, USA
  2. Cancer Center Flow Cytometry Shared Resource, University of Pennsylvania, Philadelphia, PA 19104, USA
  3. Present address: Center for Tropical and Emerging Global Diseases, and Department of Cellular Biology, University of Georgia, Athens, GA 30602, USA

Correspondence to:

David S. Roos, E-mail: droos@mail.sas.upenn.edu

Received 9 November 2000; Accepted 6 December 2000; Revised 6 December 2000

Apicomplexan parasites—including the causative agents of malaria (Plasmodium sp.) and toxoplasmosis (Toxoplasma gondii)—harbor a secondary endosymbiotic plastid, acquired by lateral genetic transfer from a eukaryotic alga. The apicoplast has attracted considerable attention, both as an evolutionary novelty and as a potential target for chemotherapy. We report a recombinant fusion (between a nuclear-encoded apicoplast protein, the green fluorescent protein and a rhoptry protein) that targets to the apicoplast but grossly alters its morphology, preventing organellar segregation during parasite division. Apicoplast-deficient parasites replicate normally in the first infectious cycle and can be isolated by fluorescence-activated cell sorting, but die in the subsequent host cell, confirming the 'delayed death' phenotype previously described pharmacologically, and validating the apicoplast as essential for parasite viability.

  • Keywords:

    • Apicomplexa,
    • apicoplast,
    • delayed death phenotype,
    • organelle segregation,
    • Plasmodium falciparum