Figure 6: Defective transmission and liver-stage maturation in ctr2− and mfs6− parasites.
From: Functional profiles of orphan membrane transporters in the life cycle of the malaria parasite

(a) Kaplan–Meier analysis of infection by intravenous injection of 10,000 (WT n=14, ctr2− n=6, mfs6− n=9) or 1,000 (mfs6− n=15) salivary gland-associated sporozoites. ***P<0.001 (Log-rank Mantel–Cox). (b) Kaplan–Meier analysis of infection by exposure to infected mosquitoes (left; WT n=3, ctr2− n=5) and subcutaneous injection of 10,000 isolated salivary gland-associated sporozoites (right; WT n=4, ctr2− n=8). ***P<0.001; **P<0.01 (Log-rank Mantel–Cox). (c) Gliding motility of ctr2− sporozoites (NS, non-significant; Mann–Whitney test). (d) Numbers of mature ctr2− and mfs6− liver stages in cultured hepatoma cells (NS, non-significant; Kruskal–Wallis with Dunn’s post test). (e) Surface areas of developing mfs6− liver-stage parasites. Shown are mean values±s.d. (NS, non-significant; Mann–Whitney test). (f) Parasite liver load in WT- and mfs6−-infected C57BL/6 mice. **P<0.01 (two-tailed Mann–Whitney). (g) Aberrant liver-stage maturation of mfs6− parasites. Shown are immunofluorescent micrographs of mature liver-stage-infected hepatoma cells. (UIS4, red; HSP70, green; Hoechst, blue). Scale bar, 10 μm. (h) Immunization/challenge protocol (top) for vaccination with genetically arrested mfs6− sporozoites. Kaplan–Meier analysis (bottom) of blood infection after sporozoite challenge infection in mfs6−-immunized mice. ***P<0.001; *P<0.05 (Log-rank Mantel–Cox).