Figure 9.

Schematic representation of the putative oligosaccharide signaling in the wild type and sitiens. In sitiens, the perception by the plant of a defective cuticle might lead to the constitutive expression of chitinases and glucan endo-1,3-β-glucosidases (1), releasing elicitor-active molecules from the fungal cell wall (2). The higher degree of methylesterification in the sitiens cell wall delivers more active host elicitors. Both types of elicitors can have a synergistic effect or even interact with each other to form even more elicitor-active complexes (3). Together with the higher permeability of the sitiens cuticle, the signaling would be faster and more effective with defense gene expression and the resistant phenotype that typifies the mutant as a consequence. In the wild type, basal expression of chitinases and glucan endo-1,3-β-glucosidases is not high enough to release elicitors from the germinating B. cinerea, and expression is induced only upon infection. The cuticle is not permeable, which delays the diffusion of signaling molecules/complexes into the cytosol of epidermal cells. Because of the absence of early signaling reactions, defense is delayed, resulting in cell wall breakdown, cell death, and fungal spreading. co, Conidium; cu, cuticle; ep, epidermal cell layer; me, mesophyll cell layer; pe, point of penetration.