Skip to main content
. Author manuscript; available in PMC: 2015 Jun 19.
Published in final edited form as: Immunity. 2014 Jun 12;40(6):924–935. doi: 10.1016/j.immuni.2014.05.006

Figure 7. The ubiquitin-like conjugation systems of the autophagy pathway are required for the localization of IFNγ effectors onto the PVM of T. gondii infection.

Figure 7

Immunofluorescence of MEFs at 2 hpi (MOI=1) of T. gondii infection with 24 hr pre-treatment of 100 U/ml of IFNγ. Representative images (left) and quantitation (right) of immunofluorescence. Irgb6 (A) and GBP1-5 (B) in WT, Atg3−/− and Atg7−/− MEFs. At least 50 of infected T. gondii were analyzed for quantitation. Statistical analysis by 1-ANOVA with Tukey post test. ****: p < 0.0001. Experiments were performed twice. Combined data as average ± SEM. (C) T. gondii and Irga6 in Atg3 WT and Atg3−/− MEFs transduced with control (GST, Glutathione-S-transferase), WT Atg3, or enzyme-null mutant (C264S). (D) T. gondii and Irga6 in Atg7 WT and Atg7−/− MEFs transduced with control (GST), WT Atg7, or enzyme-null mutant (C567A). At least 100 of infected T. gondii were analyzed for quantitation. Statistical analysis by unpaired t-test. n.s.: not significant. *: p < 0.05, **: p < 0.01. Experiments were performed twice. Combined data as average ± SEM. See also Figure S4.