Delayed death in the malaria parasite Plasmodium falciparum is caused by disruption of prenylation-dependent intracellular trafficking
Fig 6
Rab5a shows an aberrant localisation in the second IDC after clindamycin treatment.
(A) Representative live-cell images of untreated and clindamycin (5 μM) treated parasites in the second IDC following treatment are shown. Cell populations were divided into parasites with 6 or fewer nuclei (upper panel) and parasite with more than 6 nuclei (lower panel), as the disruption is clearly most pronounced in trophozoite stage parasites. GFP-Rab5a, green signal; DAPI: parasite nuclei, blue signal; merge of green and blue signal. Scale bar = 5 μm. (B) Graph showing the ratio of the brightest GFP focus fluorescence intensity to mean fluorescence intensity distributed in the parasite cytoplasm in untreated and clindamycin treated parasites. N = 38 for untreated, 1–6 nuclei; n = 52 for + clindamycin, 1–6 nuclei; n = 20 for control, > 6 nuclei and n = 16 for + clindamycin, > 6 nuclei. *P < 0.05; ***P < 0.001, Welch t test. Scatter dot plots show error bars with mean ± SD. See S2 Data for numerical data underlying figure. DAPI, 4′,6-diamidino-2-phenylindole; DIC, differential interference contrast; GFP, green fluorescent protein; IDC, intraerythrocytic developmental cycle; iRBC, infected red blood cell.