Defense activation and enhanced pathogen tolerance induced by H(2)O(2) in transgenic tobacco

Transgenic tobacco deficient in the H(2)O(2)-removing enzyme catalase (Cat1AS) was used as an inducible and noninvasive system to study the role of H(2)O(2) as an activator of pathogenesis-related (PR) proteins in plants. Excess H(2)O(2) in Cat1AS plants was generated by simply increasing light intensities. Sustained exposure of Cat1AS plants to excess H(2)O(2) provoked tissue damage, stimulated salicylic acid and ethylene production, and induced the expression of acidic and basic PR proteins with a timing and magnitude similar to the hypersensitive response against pathogens. Salicylic acid production was biphasic, and the first peak of salicylic acid as well as the peak of ethylene occurred within the first hours of high light, which is long before the development of tissue necrosis. Under these conditions, accumulation of acidic PR proteins was also seen in upper leaves that were not exposed to high light, indicating systemic induction of expression. Short exposure of Cat1AS plants to excess H(2)O(2) did not cause damage, induced local expression of acidic and basic PR proteins, and enhanced pathogen tolerance. However, the timing and magnitude of PR protein induction was in this case more similar to that in upper uninfected leaves than to that in hypersensitive-response leaves of pathogen-infected plants. Together, these data demonstrate that sublethal levels of H(2)O(2) activate expression of acidic and basic PR proteins and lead to enhanced pathogen tolerance. However, rapid and strong activation of PR protein expression, as seen during the hypersensitive response, occurs only when excess H(2)O(2) is accompanied by leaf necrosis.