Constitutive hydrolytic enzymes are associated with polygenic resistance of tomato to Alternaria solani and may function as an elicitor release mechanism

Foliar resistance to early blight disease of tomato, caused by the necrotro phic fungus Alternaria solani, is inherited in a complex quantitative manne r. Our previous studies revealed that three moderately-resistant tomato bre eding lines with different sources of early blight resistance, all possesse d higher constitutive and more rapid accumulation of PR proteins, including specific antifungal isozymes of chitinase and beta -1,3-glucanase than sus ceptible genotypes. In the present study, additional early blight resistant tomato breeding lines and susceptible genotypes were investigated for thei r constitutive levels of PR proteins. All resistant lines possessed higher constitutive levels of chitinase and beta -1,3-glucanase than susceptible g enotypes supporting earlier reported findings. Constitutive and pathogen-in duced expression of PR genes during early stages of the interaction was fou nd to be much higher in the highly resistant breeding line NC 24-E than a s usceptible line. In vitro elicitor release experiments were performed with purified ii. solani cell walls treated with constitutive total enzyme prepa rations isolated from resistant and susceptible plants. Enzyme preparations from resistant and susceptible genotypes differed in their ability to prod uce hypersensitive response (HR) elicitors from fungal cell walls: the enzy me preparations from resistant breeding lines released HR elicitors, while enzyme preparations from susceptible lines did not. Additionally, experimen ts with a partially purified preparation of basic tomato chitinases demonst rated that these enzymes were able to release HR elicitors from germinating spores of A. solani, but not mature, intact cell walls. The possibility th at constitutively produced hydrolytic enzymes may act as an elicitor-releas ing mechanism in resistance to early blight of tomato is discussed. (C) 200 0 Academic Press.