Figure 5.

Knockdown of TgUroD leads to general metabolic defects in parasites, whereas knockdown of TgCCHL1 results in selective defects in the mitochondrial ETC. A and B, whole cell ATP levels were measured in (A) rTgUrOD and (B) rHA-TgCCHL1 parasites grown in the absence of ATc (blue) or the presence of ATc for 3 days (orange). Data show the mean ± S.D. from three independent experiments (**, p < 0.01; n.s. = not significant; p > 0.05; two-tailed unpaired Student's t test). C and D, basal mOCR in (C) Tomato/TATiΔku80 parental (black/gray) and rTgUroD (green) parasites or (D) TATiΔku80 parental (black/gray) and rHA-TgCCHL1 parasites (blue) grown in the absence of ATc or the presence of ATc for 3 or 4 days. Data depict the least square means from a linear mixed model ± 95% confidence limits from three independent experiments (***, p < 0.001; n.s. = not significant; p > 0.05; ANOVA with Tukey's post hoc test). E and F, basal mOCR plotted against basal ECAR in (E) Tomato/TATiΔku80 parental (black/gray) and rTgUroD (green) parasites, or (F) TATiΔku80 parental (black/gray) and rHA-TgCCHL1 parasites (blue). Parasites were grown in the absence of ATc, or in the presence of ATc for 3 or 4 days. Data depict the least square means from a linear mixed model ± 95% confidence limits from three independent experiments.