SummaryThe roles of salicylic acid (SA) and H202 in the induction of PR proteins in tobacco have been examined. Studies were conducted on wild-type tobacco and plants engineered to express a bacterial salicylate hydroxylase capable of metabolizing SA to catechol (SH-L plants). Wildtype and PR-la-GUS-transformed plants express PR-la following challenge with Pseudomonas syringae pathovar syringae, SA or 2,6-dichloro-isonicotinic acid (INA). In contrast, SH-L plants failed to respond to SA but did express PR-la following INA treatment. H202 and the irreversible catalass inhibitor 3-amino-l,2,4-triazole (3-AT) were found to be weak inducers of PR-la expression (relative to SA) in wild-type tobacco but were unable to induce PR-la in SH-L plants, suggesting that the action of these compounds depends upon the accumulation of SA. A model has been proposed suggesting that SA binds to and inhibits a catalase inducing an increase in H202 leading to PR protein expression. Catalase activity has been measured in tobacco end no significant changes in activity following infection with P. syringae pv. syringee were detected. Furthermore, inhibition of catalass activity in vitro in plant extracts requires pre-incubation and only occurs at SA concentrations above 250 I~M. Leaf disks preincubated with I mM SA do accumulate SA to these levels and PR-la is efficiently induced but there is no apparent inhibition of catalass activity. It is also shown that a SAresponsive gene, PR-le, and a H202-sensitive gene, AoPR-1, are both relatively insensitive to 3-AT suggesting that induction of these genes is unlikely to be due entirely to inhibition of an endogenous catalase.