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Transgenic tobacco deficient in either Cat1 (Cat1AS), Cat2 (Cat2AS), or both (CatGH) was generated through sense and antisense technology. Cat1AS, Cat2AS, and CatGH plants showed no visible phenotype when grown at low light (100 µmol m −2 sec −1 . Under these conditions, deficiency in Cat1 and/or Cat2 did not lead to constitutive pathogenesis‐related (PR‐1) expression and did not potentiate PR‐1 induction by exogenous salicylic acid. This demonstrates that catalase suppression per se is not a sufficient signal for PR‐1 induction. In Cat1‐deficient plants exposed to higher light intensities (250–1000 µmol m −2 sec −1 ), PR‐1 expression was induced without pathogenic challenge and multiplication of Pseudomonas syringae pv. syringae was repressed. Yet, it is unlikely that Cat1 deficiency is mimicking the mode of action of salicylic acid in tobacco, because, concurrent with PR‐1 induction, Cat1 deficiency at high light provoked severe leaf damage, characterized by white necrotic lesions. Taken together, these results do not support the model that catalase inactivation is the key route by which salicylic acid induces PR defense responses in healthy tissue. However, because catalase deficiency is potentially lethal to leaves, catalase inactivation by salicylic acid could be of importance in the establishment of hypersensitive responses.
Chamnongpol et al. (Sun,) studied this question.