Inhibition of residual activity in the TgPKG-HA3’IT mutant by compound 2 augments the motility defect. Inhibition of residual activity in the TgPKG-HA3’IT.

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Inhibition of residual activity in the TgPKG-HA3’IT mutant by compound 2 augments the motility defect. Inhibition of residual activity in the TgPKG-HA3’IT mutant by compound 2 augments the motility defect. Motile fraction and trail lengths of the Pnative-TgPKG-HA3’IT-3′UTRexcised mutant and progenitor (Pnative-TgPKG-HA3’IT-3′UTRfloxed) strains, generated according to Fig S7, were measured by staining with α-TgSag1 antibody after compound two treatment (2 μM, 15 min). A total of 500 parasites for each strain were analyzed to calculate the motile fraction. In total, 100 trails were measured for the progenitor strain, whereas only 30 trails could be evaluated for the mutant because of severe defect (n = 3 assays, mean with SEM). Statistical significance was calculated for each pair of column individually by t test. (*P ≤ 0.05; **P ≤ 0.01; and ***P ≤ 0.001). Özlem Günay-Esiyok et al. LSA 2019;2:e201900402 © 2019 Günay-Esiyok et al.