IMC formation is disrupted in the second IDC after indolmycin treatment. Shown are representative images of immuno-fluorescence assays using anti-GAP45 (1:1,000). Untreated, indolmycin (50 μM) treated and indolmycin treated with polyprenol rescue (5 μMGGOH; geranylgeraniol) as indicated, collected in the second IDC after treatment. The IMC marker GAP45 localises atypically in indolmycin treated parasites. GGOH supplementation restores GAP45 localisation to the inner membrane complex equivalent to untreated. GAP45, green signal; DAPI, parasite nuclei, blue signal; merge of green and blue signal. Scale bar = 5 μm. BF, bright field; DAPI, 40,6-diamidino-2-phenylindole; GGOH, geranylgeraniol; IDC, intraerythrocytic developmental cycle; IMC, inner membrane complex. Following indolmycin treatment during the second IDC, GAP45 did not localise to structures that resemble IMC, suggesting that there is a defect in the assembly or trafficking of the IMC in delayed death parasites. The normal localisation of GAP45 was restored with GGOH recue treatment.

Kennedy K, Cobbold SA, Hanssen E, Birnbaum J, Spillman NJ, McHugh E, Brown H, Tilley L, Spielmann T, McConville MJ, Ralph SA. Delayed death in the malaria parasite Plasmodium falciparum is caused by disruption of prenylation-dependent intracellular trafficking. PLoS Biol. 2019 17(7):e3000376