H_2O_2 Is Involved in Hypersensitive Response and Systemic Acquired Resistance Induced by the 90 kD Protein Elicitor of Phytophthora boehmeriae

The role of H 2O 2 from the oxidative burst of tobacco leaves induced by 90 kD protein elicitor purified from the culture filtrate of Phytophthora boehmeriae in the hypersensitive response (HR) and systemic acquired resistance (SAR) of tobacco was studied. The elicitor induced a strong, biphasic H 2O 2 burst in treated leaf and the first untreated leaf. The kinetics was biphasic: phaseⅠ peaked 3 h and phaseⅡ 12 h after the treatment (Fig.3). The elicitor caused HR cell death of which the peak lagged behind the second H 2O 2 burst by 8 h (Figs.1 3). It has been shown recently that during the interaction of plants with pathogens, the expression of ROS detoxifying enzymes such as ascorbate peroxidase (APX) is suppressed, suggesting that this suppression might enhance H 2O 2 production. To examine further the role of H 2O 2 in HR cell death and SAR, The HR and SAR induced by elicitor were studied in antisense APX tobacco. Anti APX transgenic plants with reduced capability to detoxify H 2O 2 were found to be more sensitive than wild type plants to the elicitor. They exhibited HR cell death in response to low dosages of elicitor that did not trigger the activation of HR cell death in plants (Fig.4). And the transgenic plants were more resistant to tobacco black shank fungus, P.nicotianae , and TMV than the control plants after being induced by the elicitor (Figs.5 6). The results provide direct genetic evidence for H 2O 2 acting as an important signal molecule mediating elicitor induced HR cell death and SAR.