Abstract

SUMMARY The resistance of immature grape berries to Botrytis cinerea Pers. ex Fr. results from a combination of factors, among which the accumulation of the stilbene phytoalexin t-resveratrol. Stilbene accumulation is thought to be induced by oligogalacturonides (OGs) which are released from the plant cell wall during tissue maceration catalysed by polygalacturonases (PGs) produced by necrotrophic fungal pathogens. Inhibitors of PG activity, the polygalacturonase-inhibiting proteins (PGIPs), have the capability to slow the hydrolytic activity of PGs and favour the accumulation of active OGs. In the present work we have observed that artificial inoculation of grape inflorescences and immature berries at bloom and post bloom, leads to severe infection of the rachis, while lesions on young berries did not result in the development of the disease, but in the development of necrotic spots and rings. PG was detectable in berry tissues, but its secretion was significantly lower than in infected leaves. Tissues of immature berries reacted to B. cinerea inoculation by a marked accumulation of t-resveratrol. PG produced during spore germination of B. cinerea elicited t-resveratrol accumulation. Apoplastic fluids (AFs) from immature berries and leaves were found to inhibit total PG activity produced by B. cinerea, indicating the involvement of a proteinaceous or non-proteinaceous PG inhibitor, or both, as intercellular defence mechanisms. Taken together, our results suggest that the inhibition of PG produced by B. cinerea mediated by a putative PG inhibitor during the early stages of infection of immature grape berries plays a central role in promoting accumulation of t-resveratrol and, consequently, the restriction of pathogen spread.

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