Fig. 7.

TgMAPK1-mediated control of parasite proliferation is iNOS and MKK3-dependent; (a) bone marrow-derived macrophages (BMDM) from iNOS KO mice were infected with tachyzoites at a multiplicity of infection (MOI) of 0.3 and treated with IFN-γ 16 h later. Proliferation was assessed 52 h post-infection by [³H]uracil incorporation as a function of IFN-γ concentration. 100% proliferation represents [³H]uracil incorporation in the absence of IFN-γ. P value compares curves by ANOVA; (b) proliferation in the absence of exogenous IFN-γ over time. Means ± standard error of the means is shown. P value compares curves by ANOVA; (c) BMDM were infected with yellow fluorescent protein (YFP)⁺ TgMAPK1^con (con) or TgMAPK1^lo (lo) tachyzoites at a MOI of 0.3. CD11b⁺YFP⁺ (infected) cells were sorted 52 h post-infection, total RNA isolated, and quantitative RT-PCR for T. gondii HSP70 was performed, normalized to T. gondii GAPDH. The mean ± standard error of the mean is shown along with the P value (Student’s t-test); (d) BMDM from MKK3 KO mice were infected, treated, analyzed and presented as described in Fig. 5a, along with the densitometric ratios showing phospho-p38 induction (p-p38/total p38) in Table 3; (e) MKK3 KO BMDM were infected and treated with IFN-γ as described in panel (a); (f) proliferation in panel (e) in the absence of exogenous IFN-γ over time. Mean of triplicates ± standard errors of the mean is shown and P values compare curves by ANOVA.