FIGURE 1.

Schematic diagram of the interactions between the bacterial necrotroph Pectobacterium and its host plants. Pectobacterium virulence relies on macerating plant tissue through the action of PCWDEs secreted by the type I (T1) and type II (T2) secretion systems. Plant cell death is promoted by the action of toxins such as Nip and the effector DspE, which is secreted though the type III (T3) secretion system. Type IV (T4) secretion system and type VI (T6) secretion system may contribute to virulence. Plant immune responses are triggered by recognition of conserved pathogen-associated molecular patterns (PAMPs) such as flagella or damage-associated molecular patterns (DAMPs) such as OGs released by the action of PCWDEs by respective pattern recognition receptors. These recognition events in turn trigger partly overlapping defense responses including induction of defense gene expression and synthesis of various defensive compounds such as phytoalexins, defensins and PR-proteins – resulting in PTI. Bacteria can attenuate PTI particularly in the early phase of infection by tight control of PCWDE production minimizing DAMP generation. The defenses are overwhelmed at later stages by promotion of cell death and massive PCWDE production at high bacterial cell densities.