Salicylic acid (SA) is absolutely required for establishment of acquir
ed resistance in non-infected tissues following localized challenge of
other leaves with a necrotizing pathogen. Although not directly respo
nsive to SA, or induced systemically following pathogen challenge, the
expression of defence gene promoter fusions AoPR1-GUS and PAL-3-GUS a
fter wounding or pathogen challenge could be enhanced by pre-treating
tobacco plants hydroponically with SA, a phenomenon designated 'potent
iation'. Potentiation of AoPR1-GUS wound-responsiveness was also demon
strated locally, but not systemically, in tobacco tissue exhibiting ac
quired resistance following infection with either viral or bacterial p
athogens. Potentiation of wound-responsive expression by prior woundin
g could not be demonstrated. In contrast, potentiation of pathogen-res
ponsive AoPR1-GUS expression was exhibited both locally and systemical
ly in non-infected tissue. The spatial and temporal exhibition of defe
nce gene potentiation correlated directly with the acquisition of resi
stance in non-infected tissue. Pathogen-responsive potentiation was ob
tained at about 10-fold lower levels of salicylic acid than wounding-r
esponsive potentiation in AoPR1-GUS tobacco plants prefed with salicyl
ate. These results may explain the failure to observe systemic potenti
ation of the wound-responsive defence gene expression. The data sugges
t a dual role for SA in terms of gene induction in acquired immunity:
a direct one by induction of genes such as pathogenesis-related protei
ns, and an indirect one by potentiation of expression of other local d
efence genes (such as PAL and AoPR1) which do not respond directly to
SA but become induced on pathogen attack or wounding.