Delayed death in the malaria parasite Plasmodium falciparum is caused by disruption of prenylation-dependent intracellular trafficking (original) (raw)
Fig 5
Aberrant morphology of intracellular structures is prenylation dependent in delayed-death parasites.
Parasites were treated with indolmycin (50 μM), with and without polyprenol rescue (5 μM GGOH) as indicated. Enriched trophozoite-stage parasites were collected for reduced osmium fixation 72–78 hours post drug administration (equivalent to 28–32 hpi in the second IDC after treatment). (A) Representative images (top-down and cross-sectional), from SEM of each condition: untreated, indolmycin treated (+ indolmycin), and indolmycin treated with polyprenol rescue (+ indolmycin + GGOH). Structures indicated are N, DV, and CI. Scale bar = 3 μm. (B) 3D-rendered iRBCs using serial block-face scanning electron microscopy. Indicated compartments are RBC (white), parasite (blue), CIs (yellow), and DV (red). Scale bar = 3 μm. (C) Parasites were scored for number of DV compartments relative to number of nuclei in each treatment condition. Untreated: 1 nucleus n = 18, 2 nuclei n = 34, ≥ 3 nuclei n = 49; + indolmycin: 1 nucleus n = 16, 2 nuclei n = 29, ≥ 3 nuclei n = 14; + indolmycin + GGOH 1 nucleus n = 17, 2 nuclei n = 19, ≥ 3 nuclei n = 19. Scatter dot blots show error bars with mean ± SD. (D) The total volume (μm3) of the DVs and CIs were measured in each treatment condition. Bar graphs show error bars with mean ± SD. See S2 Data for numerical data underlying figure. CI, cytostomal invagination; DV, digestive vacuole; GGOH, geranylgeraniol; hpi, hours post invasion; IDC, intraerythrocytic developmental cycle; N, nucleus; RBC, red blood cell.