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. 2009 Jul 22;106(31):13004–13009. doi: 10.1073/pnas.0906387106

Fig. 2.

Fig. 2.

Phenotypic analysis of P. falciparum p52−/p36−-deficient sporozoites and liver stages reveals a severe defect in liver-stage development. (A) The p52−/p36− parasites show normal invasion of the mosquito salivary glands; no significant differences were observed between WT and the double-knockout clones (P = 0.89). (B) The p52−/p36− parasites showed slightly lower gliding activity compared with WT parasites; the effect was not statistically significant at the 95% confidence level (P = 0.11). (C) WT and p52−/p36− parasites have comparable ability to enter hepatocytes; no significant difference was seen between p52−/p36− and WT parasites (P = 0.11). (D) The double-knockout parasites show a severe developmental arrest and do not persist, because no p52−/p36− liver stages are detected at 4 days after HC-04 cell line invasion. Statistical differences between the mutant and WT parasite lines were evaluated by the Wilcoxon matched-pairs, signed-rank test. nd, not detected.