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. Author manuscript; available in PMC: 2019 Nov 20.
Published in final edited form as: Sci Signal. 2018 Nov 20;11(557):eaap9921. doi: 10.1126/scisignal.aap9921

Fig. 7. Requirement of ULK1/2 for the generation of IFNγ-dependent antiviral effects.

Fig. 7.

(A) Crystal violet viability analysis of EMCV-induced cytopathic effects in Ulk1/2+/+ and Ulk1/2−/− MEFs pretreated with IFNγ at the indicated doses for 16 hours and subsequently challenged with encephalomyocarditis virus (EMCV) for 24 hours. Data are means ± SEM of quadruplicate assays from 3 independent experiments. (B) Crystal violet viability analysis of EMCV-induced cytopathic effects in human fibrosarcoma 2fTGH cells pretreated for 2 hours with the ULK1 kinase inhibitor MRT68921 (MRT) as indicated, then exposed to IFNγ for 16 hours before challenge with EMCV for 24 hours. Data are means ± SEM of quadruplicate assays from 3 independent experiments. (C) qRT-PCR analysis of Cxcl10 (left) and Ifit3 (right) mRNA expression in Ulk1/2+/+ MEFs were treated with DMSO (vehicle-control, C), XMD8–92 (XMD), and/or IFNγ, as indicated. Data are means ± SEM from 4 independent experiments. (D) Crystal violet viability analysis of EMCV-induced cytopathic effects in human fibrosarcoma 2fTGH cells pretreated for 2 hours with the ERK5 inhibitor XMD8–92 (XMD) as indicated, then exposed to IFNγ for 16 hours before challenge with EMCV for 24 hours. Data are means ± SEM of quadruplicate assays from 3 independent experiments. (E) Schematic illustration of the potential role of ULK1/2 in IFNγ signaling. *P<0.05, **P< 0.01, ****P< 0.0001 by one-way ANOVA analysis followed by Tukey’s multiple comparisons test (C) or two-way ANOVA with Post-hoc t-tests (A, B and D).