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| The EMBO Journal
(2001) 20, 330–339, doi: 10.1093/emboj/20.3.330 |
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| A plastid segregation defect in the protozoan parasite Toxoplasma gondii |
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| Cynthia Y. He1, Michael K. Shaw1, Charles H. Pletcher2, Boris Striepen3, Lewis G. Tilney1 and David S. Roos1 |
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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 To whom correspondence should be addressed David S. Roos, droos@mail.sas.upenn.edu Received 9 November 2000; Revised 6 December 2000; Accepted 6 December 2000. |
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| Abstract |
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| 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. |
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| Keywords: Apicomplexa, apicoplast, delayed death phenotype, organelle segregation, Plasmodium falciparum |
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