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. 2023 May 18;11(3):e00104-23. doi: 10.1128/spectrum.00104-23

FIG 3.

FIG 3

PP2Acα deficiency compromises the intracellular growth and virulence of Toxoplasma gondii tachyzoites. (A) Newly isolated tachyzoites were treated with 0 nM, 50 nM, or 2 μM okadaic acid (OA). Their attachment, invasion, and invasion efficiency into HFF-1 cells were assayed. *, P ≤ 0.05; ***, P ≤ 0.001, all by t tests. (B) The numbers of tachyzoites per parasitophorous vacuole in HFF-1 cells as an indicator of intracellular replication followed by OA treatment, as described in panel A. At least 50 vacuoles are analyzed for each group. ***, P ≤ 0.001, by a two-way ANOVA. (C) The numbers and areas of plaques formed by 0 nM, 50 nM, or 2 μM OA-treated tachyzoites. ***, P ≤ 0.001, both by t tests. (D) The attachment, invasion, and invasion efficiency of the tachyzoites of wild-type (WT), PP2Acα knockout (ΔPP2Acα), and its complemented (::PP2Acα) cells to HFF-1 cells. **, P ≤ 0.01; ***, P ≤ 0.001, all by t tests. (E) The numbers of tachyzoites per parasitophorous vacuole in HFF-1 cells of WT, ΔPP2Acα, and ::PP2Acα tachyzoites. At least 50 vacuoles were analyzed for each mutant. **, P ≤ 0.01; ***, P ≤ 0.001, by a two-way ANOVA. (F) The numbers and areas of plaques formed by WT, ΔPP2Acα, and ::PP2Acα tachyzoites. ***, P ≤ 0.001, both by t tests. (G) The survival rate of ICR mice infected with WT, ΔPP2Acα, and ::PP2Acα tachyzoites (100 tachyzoites per mouse, 10 mice per group). *, P ≤ 0.05; ***, P ≤ 0.001.