\"or PfPMRT1, a minor growth delay was measurable, which resulted in a significantly reduced parasitemia at day 3 upon knockdown using 2.5 mM glucosamine (two-tailed Wilcoxon rank sum test, W = 15, n1 = 5, n2 = 3, P = 0.03), but was not significant when using 5 mM glucosamine (two-tailed Wilcoxon rank sum test, W = 10, n1 = 4, n2 = 3, P = 0.16) (Fig. 2E). Additionally, significantly fewer newly formed ring stage parasites were observed at 84 h postinvasion (hpi) (Fig. 2F), and multiple pairwise post hoc comparisons using the Conover-Iman rank sum test and Benjamini-Hochberg method to control the false discovery rates showed significant stepwise reductions of ring stage parasites after induction of glmS-based knockdown of PfPMRT1 using both 2.5 mM glucosamine (adjusted P = 0.0078) and 5 mM glucosamine (adjusted P = 0.0005) in comparison to untreated control cell cultures.\"

\"In contrast to the glmS-based knockdown experiment, DiCre-based gene excision (induced by the addition of rapalog to young ring stages of condΔPMRT1 parasite cell cultures) abolished growth within the first replication cycle (Fig. 3F; Fig. S5A). \" \"Loss of the PPM-localized PfPMRT1 leads to an arrest of parasite development at the trophozoite stage and the formation of PPM-derived protrusions.\" \"Depletion of PfPMRT1 results in an early arrest of gametocyte development.\"

\"In contrast to the glmS-based knockdown experiment, DiCre-based gene excision (induced by the addition of rapalog to young ring stages of condΔPMRT1 parasite cell cultures) abolished growth within the first replication cycle (Fig. 3F; Fig. S5A). \" \"Loss of the PPM-localized PfPMRT1 leads to an arrest of parasite development at the trophozoite stage and the formation of PPM-derived protrusions.\" \"Depletion of PfPMRT1 results in an early arrest of gametocyte development.\"