Dextran as an elicitor of phenylpropanoid and flavonoid biosynthesis in tomato fruit against gray mold infection.

Alpha-1,3-glucan is often synthesized on the surface of pathogenic filamentous fungi cell walls to block pathogen-associated molecular patterns (PAMPs) generation by host plant enzymes and the subsequent immune system response of the plant. Here, Botrytis cinerea susceptibility was assessed in tomato fruit to determine whether the fruit could recognize this camouflage and mount an immune response to it. The results showed that local mechanical wounds treated with dextran and laminarin, except amylopectin, could locally and then systemically activate disease resistance against B. cinerea infection in tomato fruit. Dextran treatment effectively elicited fruit callose deposition and phenylpropanoid and flavonoid biosynthesis to a greater extent than α-glucanase activity relative to the mock group surface wounds. Enzymatic hydrolysis of this polysaccharide provided some help in improving host disease resistance. Taken together, these results demonstrate that tomato fruit can perceive α-1,3-glucan as a kind of PAMPs but have limited ability to degrade it.

Depression of Fungal Polygalacturonase Activity in Solanum lycopersicum Contributes to Antagonistic Yeast-Mediated Fruit Immunity to Botrytis.

The acquisition of susceptibility to necrotrophy over the course of ripening is one of the critical factors limiting shelf life. In this study, phytopathology and molecular biology were employed to explore the roles of pectinase in fruit susceptibility and ripening. Solanum lycopersicum fruit softened dramatically from entirely green to 50% red, which was accompanied by a continuously high expressed SlPG2 gene. The necrotrophic fungus Botrytis cinerea further activated the expression of SlPGs and SlPMEs to accelerate cell wall disassembly, while most of the polygalacturonase inhibitor proteins encoding genes expression were postponed in ripe fruit following the pathogen attack. Pectin induced the antagonistic yeast to secrete pectinolytic enzymes to increase fruit resistance against gray mold. The activities of pathogenic pectinase of B. cinerea were correspondingly depressed in the pectin-inducible yeast enzyme elicited ripe fruit. These data suggest that pectinase is a molecular target for regulation of disease resistance during fruit ripening.