A plastid segregation defect in the protozoan parasite Toxoplasma gondii

Apicomplexan parasites-including the causative agents of malaria (Plasmodiu m sp,) and toxoplasmosis (Toxoplasma gondii)-harbor a secondary endosymbiot ic plastid, acquired by lateral genetic transfer from a eukaryotic alga, Th e 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 fluorescen t protein and a rhoptry protein) that targets to the apicoplast but grossly alters its morphology, preventing organellar segregation during parasite d ivision. Apicoplast-deficient parasites replicate normally in the first inf ectious cycle and can be isolated by fluorescence-activated cell sorting, b ut die in the subsequent host cell, confirming the 'delayed death' phenotyp e previously described pharmacologically, and validating the apicoplast as essential for parasite viability.