Mechanism of resistance of avocado fruits to Colletotrichum gloeosporioides attack.
Prusky, D.; Ardi, R.; Kobiler, I.; Beno-Moalem, D.; Leikin, A.;
ACIAR Proceedings Series Year: 1998 Issue: No. 80 Pages: 63-71 Ref: 10 ref.
1998
บทคัดย่อ
C. gloeosporioides [Glomerella cingulata] is a destructive postharvest pathogen of avocado and other tropical fruits. The pathogen infects tropical fruits throughout the period of fruit growth, but remains quiescent for weeks or months while the fruit is immature. Conidia of the fungus germinate on the peel of avocado fruit, producing appressoria. The appressoria produce infection pegs that breach the wax layer and come to rest on the underlying epidermal cells. Upon harvest and fruit ripening, quiescent infections are activated, causing extensive damage to the fruit. Quiescent infection appears to be a fungal response to adverse physiological conditions temporarily imposed by the host. The lack of available nutrients, the presence of preformed antifungal compounds and the lack of enzymatic potential have been tested as possible causes of quiescent fungal infections on unripe fruits. The quiescence of G. cingulata in unripe avocado fruit has been attributed to the presence of high concentrations
of several preformed antifungal compounds, the most active of them 1-acetoxy-2-hydroxy-4-oxoheneicosa-12, 15-diene. Concentrations of the antifungal diene and epicatechin (a non-specific inhibitor present in the pericarp of unripe fruits but not ripe fruits) decrease during fruit ripening and were accordingly suggested as major factors in permitting activation of quiescent infections. The catabolism of the diene after harvest is attributed to the oxidation by lipoxygenase whose activity is in turn regulated by epicatechin. The level of epicatechin is a critical point regulating the mechanism of resistance. Induction of epicatechin level enhances the level of the antifungal compounds by preventing its breakdown. Induced levels of epicatechin occur by activation of the phenylpropanoid pathway with enhanced activity of phenylalanine ammonia lyase, chalcone synthase, and flavanone 3 hydroxylase. G. cingulata also decays the mesocarp of peeled unripe fruits despite fungitoxic concentrations of the antifungal com
pounds. This may be explained by the compartmentalisation of the antifungal diene in idioblast oil cells. These idioblasts are metabolically active and can incorporate labelled precursors and synthesis and export diene. Modulation of the level of preformed antifungal compounds could become a basis for enhancing resistance and reducing pesticide use.