Fig. 3: PWWP3A deficiency potentiates RNA virus-triggered signaling.

a The control (con.) and PWWP3A-knockout (KO) HEK293 cells were uninfected or infected (blank) with sendai virus (SeV, orange) for 8 h before RT-qPCR analysis (n = 3 biological replicates per group). b The control and PWWP3A-KO HEK293 cells were infected with SeV at the indicated time, then the indicated total or phosphorylated proteins were detected by immunoblotting analysis with the indicated antibodies. c Cell fractionation analysis of the IRF3 nuclear translocation in control and PWWP3A-KO HEK293 cells infected with SeV at the indicated time points. Pwwp3a^+/+ (blue) and Pwwp3a^−/− (orange) bone marrow-derived macrophages (BMDMs) were infected with SeV (d, g), vesicular stomatitis virus (VSV) (e, g) or herpes simplex virus type 1(HSV-1) (f, g) at the indicated time points before RT-qPCR analysis (n = 3 biological replicates per group). Pwwp3a^+/+ and Pwwp3a^−/− BMDMs were infected with SeV (h) or HSV-1 (i) at the indicated time points, then the indicated total or phosphorylated proteins were detected by immunoblotting analysis with the indicated antibodies. The levels of pIRF3 and pTBK1 were quantified using the Chemiluminescence-Imaging program and normalized to the levels of IRF3 and TBK1, respectively (b, h, i). Graphs shown as mean ± SD, p values are from one-way ANOVA (a) or two-tailed, unpaired t-test (d–g). At least three independent experiments were performed with similar results. Source data are provided as a Source Data file.