Fig. 7: Model of P7 positively regulates the MPK3/6 pathway and inhibits callose-dependent antiviral defence, thereby promoting ToCV infection.

Under normal condition (left column), the MPK3/6 was inactive, and the callose was localized in the cell wall. Upon ToCV infection (right column), the MPK3/6 was activated. ToCV P7 interacts with NbMPK3/6 and inhibits the entry of NbMPK3/6 into the nucleus. P7 then inhibits the immune response mediated by NbMPK3/6 and promotes ToCV replication. Subsequently, NbMPK3/6 phosphorylates P7 at S59. The phosphorylated P7 and NbMPK3 then localized to the plasma membrane. The phosphorylated P7 targets NbREM1.1 at the plasma membrane to inhibit its callose-inducing activity to promote ToCV movement in N. benthamiana plants.