Fig 1. The availability of AGO1 has a significant impact on PVA infection and HCPro is responsible for taming AGO1’s antiviral effects.

A-C) The effect of silencing of AGO1 on PVA^WT gene expression (A), particle accumulation (B) and vRNA level (C) in locally infected leaves. D-F) The effect of AGO1 overexpression on PVA^WT gene expression (D), particle accumulation (E) and vRNA level (F) in locally infected leaves. G, H) The effect of silencing (G) and overexpression (H) on PVA^ΔHCPro vRNA levels in locally infected leaves. PVA^WT or PVA^ΔHCPro and firefly luciferase were co-infiltrated at OD₆₀₀ 0.005 and 0.01, respectively with either the silencing constructs (OD₆₀₀ 0.4) or the overexpression constructs (OD₆₀₀ 0.3). Samples were taken from the infiltrated leaves at 5 dpi. Viral gene expression was measured with the dual luciferase assay after which PVA^WT-derived Renilla luciferase activity was normalized to firefly luciferase activity. The abundance of encapsidated viral genomes was determined by IC RT-PCR and the level of viral RNA was likewise measured by RT-PCR. RLUC and immunocapture data is presented as means of at least three independent experiments. RNA levels are representative results of three independent experiments. See also S1 Fig for AGO1 and AGO2 mRNA expression levels. Error bars denote standard deviation and student’s t-test was used to calculate statistical significance (* P<0.05, ** P<0.01, *** P<0,001).