Virus infection facilitated by virus-encoded effector proteins. A and B) Suppression of PTI by MP. A) Perception of dsRNA produced in cortical ER-associated VRCs at the PM by an unknown membrane-associated or intracellular PRR and the SERK1 coreceptor (with potential contribution by one or more other coreceptors) triggers a signaling pathway leading to callose deposition and PD closure. dsRNA produced during infection in the VRC may require secretion into the apoplasm (1) to allow perception at the PM. Externally applied poly(I:C) may be perceived from the apoplasm (2) or secreted upon initial uptake by the cells (3). Viral dsRNA as well as poly(I:C) may also be sensed by an intracellular cytoplasmic PRR, or by an internalized SERK–PRR complex, as shown in the figure in endosomes, shown as a gray vesicle. B) MP suppresses dsRNA-triggered callose deposition and allows intercellular spread of the viral ribonucleoprotein complex (vRNP). The MP may inhibit dsRNA sensing by the intracellular dsRNA receptor or internalized SERK-PRR complex (1), interact with intracellular PTI signaling (2) or modify the activity of callose synthesizing or degrading enzymes at PD (3). The MP may also be secreted to inhibit dsRNA perception at the PM (4). C) dsRNA triggers PTI and antiviral RNA silencing and both responses are suppressed by viral effector proteins to support virus propagation. Whereas MP acts in cells at the virus front to facilitate virus movement by blocking a dsRNA-induced callose defense response at PD, the VSR blocks dsRNA-induced antiviral RNA silencing in the center of infection sites to support virus replication and production of virus progeny. A local infection site of TMV encoding MP fused to GFP (TMV-MP:GFP, 7 dpi) in N. benthamiana is shown. Scale bar, 1 mm.