Fig. 2: OGT inhibits IAV infection via both catalytic activity-dependent and -independent manner in human cells.

a–d OGT-KO HT29 cells were reconstituted with empty vector (EV), GFP-tagged OGT (OGT-WT) or its K908A mutants, followed by the infection with PR8 virus at a MOI = 1 for 12 h. Viral mRNAs (a), and viral titers (b) were measured by RT-PCR, and TCID₅₀ assays respectively. c Gene transcripts including IFNA4, IFNB, MX1, ISG15, IL6, and TNFA in the cells were measured with RT-PCR. d Immunoblotting of phosphorylated TBK1, IRF3, IKKα/β, IκBα, and NF-κB signaling molecules and protein O-GlcNAcylation was performed with indicated antibodies. e–h, MAVS-KO or IRF3-KO and WT control of HT29 EV, OGT-WT and OGT-K908A cells were infected with PR8 virus at a MOI = 1 for 12 h. e The expression of MAVS and IRF3 proteins in cells were assessed by immunoblotting. Viral mRNAs (f), and viral titers (g) were measured by RT-PCR and TCID₅₀ assays respectively. h Gene transcripts including IFNB, MX1, ISG15, IL6, and TNFA in the cells were measured with RT-PCR. Data are representative of three independent experiments (a–c and f–h). Statistical significance was determined by two-way ANOVA followed by Tukey’s test (a–c and f–h), P values of statistical comparisons are shown in each graph. The error bars represent SEM from n = 3 independent biological replicates (a–c and f–h). Source data are provided as a Source Data file.