Fig 1: IFNγ’s pro-persistence and PRMTi’s antipersistence effects in PC9 cells depend on STAT1.(A) Relative Erl persistence of STAT1+/+, STAT1+/−, or STAT1−/− cells in ± IFNγ, normalized to − IFNγ (n = 5). (B) Relative Erl persistence of STAT1+/+ (left) or STAT1−/− (right) cells in ± MS023 ± IFNγ, normalized to − MS023 ± IFNγ (n = 3). STAT1 protein level (C) and mRNA level (D) of cells in ± GSK3368715 (GSK715) for 3 days, followed by ± IFNγ (5 ng/ml) for 1 day. (E) Relative intensity of unmodified, monomethylated, and dimethylated PABP2 peaks in mass spectrometry with cells in ± MS023 (5 μM) for 3 days. (F) STAT1 protein level of cells with ± PABP2 knockdown (siPABP2) for 3 days, followed by ± IFNγ (5 ng/ml) for 1 day. (G) P-STAT1 intensity ratio (N/C: nuclear versus whole cell) of cells in ± GSK715 for 3 days, followed by ± IFNγ (2 ng/ml) for 1 day. Shown are averages of single cell results in replicate wells (n = 3; >1000 cells per well). IRF1 mRNA level (H) and protein level (I) of cells in the same treatment as in (D) and (G), respectively. IRF1 intensity in whole cell was measured. (J) Relative Erl persistence of cells with (siIRF1) or without (siNC) knockdown for 2 days, followed by persister assays in ± IFNγ; normalized to − IFNγ with siNC (n = 5). (A to J) Erl: 2.5 μM. Error bar: SD. Unpaired, two-tailed t tests: ns, P > 0.05; *P ≤ 0.05; **P ≤ 0.01; ***P ≤ 0.001; ****P ≤ 0.0001. (C and F) Loading controls: Glyceraldehyde-3-phosphate dehydrogenase (GAPDH).