Control of Fruit Cracking by Shaping Skin Traits – Apple as a Model

Abstract

Skin cracking limits fruit quality and marketability. Suggested causes are environmental conditions, orchard management, and failure of the skin to resist surface tension due to fruit expansion. Fruit skin is made up of epidermis cells and cuticular matrix. Theoretical and experimental studies of skin mechanics, together with anatomical and molecular comparisons of cracking-susceptible vs. tolerant genotypes, suggest that increased cuticle thickness, high epidermal cell density and strong adhesion between neighboring cells are associated with cracking resistance. Calyx-end cracking disorder in apple is treated with a mixture of gibberellic acids 4 and 7 (GA4 + 7) and the cytokinin 6-benzyladenine (BA) early in fruit development. The treatment not only significantly reduces cracking incidence in the orchard, it also provides information on the cellular and molecular factors determining fruit-skin resistance to growth strain. BA + GA4 + 7 application results in an immediate increase in epidermal cell density that is maintained until fruit maturation. Moreover, the epidermal cells form clusters within the cuticular matrix, which may strengthen the cuticle by adding more cell-wall components and may enhance crack repair. Skin anatomical modifications are complemented by the expression of genes associated with epidermal cell patterning and cuticle formation. Gene-networking analysis supports the interaction between cell-wall synthesis, cuticle-formation, and GA-signaling gene clusters. Overall, data suggest that BA + GA4 + 7 treatment does not modify developmental cues, but promotes or enhances the innate developmental program. This review presents data on BA- and GA4 + 7-induced skin modifications that complement previously suggested models for cracking resistance in fruit. Knowledge gained on apple fruit skin traits may be applied to control cracking in other fruit as well.