Figure 2.

Possible mechanisms of cell conditioning by nonviral factors induced by cell wall trauma and the specific effects of virus-directed MP, leading to the creation of favorable conditions for the intercellular spread of infection. Cell wall damage (1) results in the activation of pre-existing PME (2a) as well as PME expression (2b), leading to the increased release of gaseous methanol (3). Methanol-induced genes (MIGs), including β-1,3-glucanase (BG) and NCAPP, are stimulated by methanol (4). MIG induction activates intercellular transport increasing the Pd SEL: BG degrades callose around Pd (4a), and NCAPP is believed to be indispensable for MP functioning. TMV penetrates into the cell through damage to the cell wall, starts to replicate, and forms viral replication complexes (VRCs) on ER membranes (5). MP translated from genomic and subgenomic vRNAs is delivered to the Pd in a tight connection with ER membranes (6a) and possibly via the Golgi apparatus in a PME-mediated manner (6b). As MP colocalizes with SYTA in the VRC and Pd, the mechanisms of SYTA transport to the Pd may influence MP delivery. MP may participate in the displacement of negative regulators from the Pd structure and the activation of positive regulators (e.g., SYTA). (7) Moving independently of the genomic viral RNA to the neighboring cells MP increases Pd SEL and creates favorable conditions for the intercellular spread of infection.