Fig. 2: PRMT9 deficiency in primary peritoneal macrophages enhances RLRs-triggered IFN-β signaling.
From: The protein arginine methyltransferase PRMT9 attenuates MAVS activation through arginine methylation
a, b ELISA quantification of IFN-β secretion and (a–c) qRT-PCR analysis of Ifnb1, Ifna4, Cxcl10 mRNA in Prmt9CKO and Prmt9WT peritoneal macrophages infected with a SeV or b stimulated with 5′-pppRNA or infected with c HSV-1 (mean ± SD, two-tailed student’s t-test Prmt9CKO vs. Prmt9WT, for a, Ifnb1: ***p = 0.0002, ***p = 0.0004, **p = 0.0052 in sequence; Ifna4: *p = 0.0140, ****p < 0.0001, **p = 0.0088 in sequence; Cxcl10: **p = 0.0078, 0.0076, 0.0017 in sequence; IFN-β: **p = 0.0012, 0.0081, 0.0015 in sequence, n = 3 independent experiments. For b: Ifnb1: **p = 0.0011, ***p = 0.0003, ***p = 0.0008 in sequence; Ifna4: ***p = 0.0002, **p = 0.0020, **p = 0.0034 in sequence; Cxcl10: *p = 0.0139, **p = 0.0013, ***p = 0.0008 in sequence; IFN-β: **p = 0.0034, 0.0024, 0.0024 in sequence, n = 3 independent experiments). d qRT-PCR analysis of Ifnb1 (left), VSV mRNA (middle), plaque assay of VSV titers (right) and immunoblot analysis of VSV-G (far right) in Prmt9CKO and Prmt9WT peritoneal macrophages infected with VSV (MOI, 0.1) for 0–12 h (mean ± SD, two-tailed student’s t-test Prmt9CKO vs. Prmt9WT, ****p < 0.0001, ***p = 0.0005, ****p < 0.0001 in sequence, n = 3 independent experiments). e For the densitometric analysis (right), the values were normalized to actin (mean ± SD, two-tailed t-test Prmt9CKO vs. Prmt9WT, *p = 0.0248, **p = 0.0020, 0.0046 in sequence, n = 3 independent experiments). Line graphs were presented relative to the second lane. The qRT-PCR and ELISA results are presented relative to those of untreated wild-type cells (Average of three replicates, a–d). *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001; ns not significant (two-tailed Student’s t-test).
