Natural disease resistance in strawberry fruit and Geraldton waxflower flowers

Antifungal activity against Botrytis cinerea and Cladosporium cladosporioides declined with increasing fruit maturity as shown by thin layer chromatography (TLC) bioassay. Preformed antifungal activity was also demonstrated in flower tissue. Decline in fruit antifungal compounds was correlated with a decline in natural disease resistance (NDR) against B. cinerea. Crude extracts of green stage I fruit contained at least two previously unreported preformed antifungal compounds (Rf = 0.44 and 0.37) that were not present in white and red stage fruit. These compounds were confirmed by TLC reagent sprays not to be phenolics or alkaloids. Positive reactions to Ehrlich’s reagent suggested that Rf = 0.37 was a teipene. The majority of antifungal activity was found in the achenes of green stage I fruit. However, antifungal activity was found in all tissue types (viz. pith, cortex, epidermis) of green stage I fruit. TLC bioassays showed that all fruit stages showed antifungal activity at the origin (Rf = 0.00). The approximate area of fungal inhibition at origin in green stage 1 fruit extracts was 90 and 70% greater than in white and red stages. TLC reagent sprays confirmed that antifungal compounds at origin contain phenolics. This is consistent with previously reported phenolic compounds in strawberry fruit that are inhibitory to B. cinerea. An investigation into the potential of enhancing NDR using different chemical (acibenzolar), biological (Aureobasidium pullulons) and physical (UV-C) elicitors was conducted with a view to developing an integrated pest management (EPM) strategy. The most promising results were achieved with pre-harvest treatments of the chemical plant activator acibenzolar. Seven glasshouse trials were conducted over a three year period. Preharvest application of acibenzolar (0.25 - 2.0 mg AI ml'1) were effective in suppressing grey mould on strawberry fruit harvested from winter grown plants. Conversely, acibenzolar was ineffective at suppressing grey mould on fruit harvested from summer grown plants. However, where acibenzolar was effective, disease development was delayed by as much as 2 days. This delay was equivalent to a 15-20% increase in shelf-life. If systemic acquired resistance and/or other inducible mechanisms are to be implemented as part of an IPM strategy for controlling B. cinerea more research is required on how environment and management factors affect the efficacy of elicitors such as acibenzolar. Geraldton waxflower is the most economically important native Australian cut flower export. Infection of Geraldton waxflower by B. cinerea can lead to unacceptable levels of flower abscission after harvest. Thus, an investigation was conducted into the nature and identities of constitutive antifungal compounds in imported Geraldton waxflower flower and leaf tissues. Antifungal activity against B. cinerea and C. cladosporioides was observed in both Geraldton waxflower leaf and flower tissue. Leaf tissue contained considerably less antifungal activity than flower tissue. Some antifungal compounds were common to the three different waxflower cultivars studied. Through TLC reagent sprays and NMR GC-MS spectra, these antifungal compounds were identified as the sesquiterpenes, globulol and grandinol. There were also at least two unidentified phenolics. Notwithstanding similarities in antifungal profiles, it was also evident from TLC bioassays that significant variations exist between different waxflower cultivars. Further work is required to fully characterise the preformed antifungals compounds found in strawberry and Gerladton waxflower tissues and to elucidate pathways involved in their biosynthesis. In addition, work is also required to look at the full spectrum of antifungal activity of these antifungal compounds. Such information will allow precise definition of the roles that these compounds may play in suppression of in strawberry and waxflower NDR against B. cinerea. In turn, this knowledge should enable the introduction of improved and/or novel IPM strategies that enhance levels of these compounds.