Systemic acquired resistance (SAR) to Sclerotinia sclerotiorum was induced in mature kiwifruit vines after localized treatment with 0.2m M salicylic acid (SA) or previous inoculation with the same pathogen. SAR was expressed in adjacent untreated leaves as a reduction in lesion diameter. SA and the pre-inoculation treatment each induced significant resistance (c. 35 and 25% reduction, respectively) in the adjacent leaves in the direction of the trunk. However no effect was seen in the adjacent leaves in the direction of the shoot tip. Radiolabel from locally applied 14 C-SA moved into the shoot and towards the trunk without accumulating in the adjacent leaves. This suggests that SA was not the primary systemic signal for SAR. Induction of SAR by S. sclerotiorum was preceded by endogenous accumulation of SA in treated and adjacent leaves. Free SA increased by three-fold after 24h in the inoculated leaf and by two-fold in the adjacent leaves after 96h. However, PAL activity did not increase locally until 48h post-inoculation and remained unchanged throughout the experiment in adjacent leaves. Therefore the signal promoting SA accumulation must either operate downstream of PAL in the SA biosynthetic pathway, or produce SA by an independent mechanism, such as the hydrolysis of stored conjugated SA.