Fig. 7: Co-condensation of TRIM25 and G3BP1 inhibits SeV virus replication.
From: TRIM25 predominately associates with anti-viral stress granules
a–d WT (V2) or TRIM25 KO HEK293T cells were transfected with indicated plasmids, and then infected with SeV. a SeV mRNA level was determined 16 h post infection. The mRNA levels of host IFNβ (b), CXCL10 (c), and ISG56 (d) were determined 12 h post infection using qRT-PCR. SeV (−) vs. SeV (+): p value: <0.001 (a–d), V2 (+) vs. TRIM25 KO (+): p value: <0.001 (a–d), SeV (−) vs. SeV (+): p value: <0.001 (a–d), TRIM25 KO-Vector (+) vs. TRIM25 KO-TRIM25 WT (+): p value: <0.001 (a–d), TRIM25 KO-TRIM25 WT (+) vs. TRIM25 KO-TRIM25 ΔPTFG (+): p value: <0.001 (a–d). e A model showing how the co-condensation between G3BP1 and TRIM25 promotes the formation of antiviral SGs. This enhances TRIM25-mediated ubiquitination of many substrates, and could activate multiple antiviral pathways, such as the RIG-I pathway and ZC3HAV1-mediated RNA degradation. All data are representative of at least three independent experiments (a–d). Mean ±s.d., statistical analysis was performed using one-way ANOVA (a–d).
