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Salicylic acid (SA) is absolutely required for establishment of acquired resistance in non-infected tissues following localized challenge of other leaves with a necrotizing pathogen. Although not directly responsive to SA, or induced systemically following pathogen challenge, the expression of defence gene promoter fusions AoPR1—GUS and PAL-3—GUS after wounding or pathogen challenge could be enhanced by pre-treating tobacco plants hydroponically with SA, a phenomenon designated ‘potentiation’. Potentiation of AoPR1—GUS wound-responsiveness was also demonstrated locally, but not systemically, in tobacco tissue exhibiting acquired resistance following infection with either viral or bacterial pathogens. Potentiation of wound-responsive expression by prior wounding could not be demonstrated. In contrast, potentiation of pathogen-responsive AoPR1—GUS expression was exhibited both locally and systemically in non-infected tissue. The spatial and temporal exhibition of defence gene potentiation correlated directly with the acquisition of resistance in non-infected tissue. Pathogen-responsive potentiation was obtained at about 10-fold lower levels of salicylic acid than wounding-responsive potentiation in AoPR1—GUS tobacco plants prefed with salicylate. These results may explain the failure to observe systemic potentiation of the wound-responsive defence gene expression. The data suggest a dual role for SA in terms of gene induction in acquired immunity: a direct one by induction of genes such as pathogenesis-related proteins, and an indirect one by potentiation of expression of other local defence genes (such as PAL and AoPR1) which do not respond directly to SA but become induced on pathogen attack or wounding.