TRANSGENIC TOBACCO WITH A REDUCED CATALASE ACTIVITY DEVELOPS NECROTICLESIONS AND INDUCES PATHOGENESIS-RELATED EXPRESSION UNDER HIGH LIGHT

Transgenic tobacco deficient in either Cat1 (Cat1AS), Cat2 (Cat2AS), o r both (CatGH) was generated through sense and antisense technology. C at1AS, Cat2AS, and CatGH plants showed no visible phenotype when grown at low light (100 mu mol m(-2) sec(-1)). Under these conditions, defi ciency in Cat1 and/or Cat2 did not lead to constitutive pathogenesis-r elated (PR-1) expression and did not potentiate PR-1 induction by exog enous salicylic acid. This demonstrates that catalase suppression per se is not a sufficient signal for PR-1 induction. In Cat1-deficient pl ants exposed to higher light intensities (250-1000 mu mol m(-2) sec(-1 )), PR-1 expression was induced without pathogenic challenge and multi plication of Pseudomonas syringae pv, syringae was repressed. Yet, it is unlikely that Cat1 deficiency is mimicking the mode of action of sa licylic acid in tobacco, because, concurrent with PR-1 induction, Cat1 deficiency at high light provoked severe leaf damage, characterized b y white necrotic lesions. Taken together, these results do not support the model that catalase inactivation is the key route by which salicy lic acid induces PR defense responses in healthy tissue. However, beca use catalase deficiency is potentially lethal to leaves, catalase inac tivation by salicylic acid could be of importance in the establishment of hypersensitive responses.