During infection, plant viruses replicate and transport their genomes to adjacent cells via cell wall nanochannels called plasmodesmata (PD).Double-stranded RNA (dsRNA), an intermediate of viral replication, acts as a viral pathogen-associated molecular pattern (PAMP), leading to the activation of pattern-triggered immunity (PTI) that restricts viralcell-to-cell movementby causing callose deposition and closure of PD. However, viruses suppress this host PTI responsewith their movement proteins, as was shown for the MPs of different tobamoviruses.Previously we showed that bak1 mutants are hypersusceptible to viruses but whether this lack of antiviral resistance is due to failure to activate PTI in response to dsRNA has not yet been tested. Here we show that bak1-4 mutants show an enhanced efficiency in systemic virus movement and are unable to develop resistance upon exogenous treatment with the synthetic dsRNA analogpoly(I:C). Moreover, previously we demonstrated that Plasmodesmata Located Proteins1,2 and 3 (PDLP1,2,3) are required for dsRNA-induced callose deposition at PD. Here we show that similar to bak1-4 mutants, also the pdlp1,2,3 mutants allow more efficient virus movement and do not activate antiviral resistance in response to poly(I:C). These findings underscore the role of dsRNA sensing and PTI signaling to PD in antiviral resistance against viruses.
