Delayed death in the malaria parasite Plasmodium falciparum is caused by disruption of prenylation-dependent intracellular trafficking
Fig 4
Indolmycin treated parasites aberrantly internalise F-dextran from preloaded RBCs in the second IDC after treatment.
Uninfected RBCs were preloaded with F-dextran by gentle hypotonic lysis and resealing. Following this, enriched and synchronised schizont-stage parasites were added to the loaded RBCs and merozoites were allowed to reinvade. Newly invaded ring-stage parasites were treated with indolmycin (50 μM), with and without polyprenol (5 μM GGOH) rescue as indicated. (A) Representative live-cell images taken 72–78 hours after drug administration are shown (equivalent to 28–32 hpi in the second IDC after treatment). F-dextran, green signal; Hoechst: parasite nuclei, blue signal; merge: BF and blue signal. Scale bar = 5 μm. (B) The number of F-dextran compartments per iRBC were scored in three independent experiments. **P < 0.01, one-tailed Student t test. Scatter dot plot shows error bars with mean ± SD. See S2 Data for numerical data underlying figure. BF, bright field; F-dextran; fluorescein dextran; GGOH, geranylgeraniol; hpi, hours post invasion; IDC, intraerythrocytic developmental cycle; ns, not significant; RBC, red blood cell.