A plastid segregation defect in the protozoan parasite Toxoplasma gondii
AUTOR(ES)
He, Cynthia Y.
FONTE
Oxford University Press
RESUMO
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.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=133478Documentos Relacionados
- Daughter Cell Assembly in the Protozoan Parasite Toxoplasma gondii
- A selector of transcription initiation in the protozoan parasite Toxoplasma gondii.
- Biosynthesis of Glycosylphosphatidylinositol Is Essential to the Survival of the Protozoan Parasite Toxoplasma gondii
- Induction of an acrosomal process in Toxoplasma gondii: Visualization of actin filaments in a protozoan parasite
- Toxoplasma gondii: a protozoan for the nineties.