Continuous
ethylene supplementation suppresses postharvest sprouting, but it can increase reducing
sugars, limiting its use as an alternative to
chlorpropham for processing potatoes. To elucidate the mechanisms involved, tubers were treated after curing with or without the
ethylene binding inhibitor
1-methylcyclopropene (1-MCP at 1 μL L-1 for 24 h), and then stored in air or air supplemented with continuous
ethylene (10 μL L-1). Across three consecutive seasons, changes in tuber physiology were assessed alongside transcriptomic and metabolomic analysis. Exogenous
ethylene alone consistently induced a respiratory rise and the accumulation of undesirable reducing
sugars. The transient respiratory peak was preceded by the strong upregulation of two genes encoding
1-aminocyclopropane-1-carboxylate oxidase (ACO), typical of
wound and stress induced
ethylene production. Profiles of parenchymatic tissue highlighted that
ethylene triggered
abscisic acid (ABA) catabolism, evidenced by a steep fall in ABA levels and a transient rise in the catabolite
phaseic acid, accompanied by upregulation of transcripts encoding an
ABA 8'-hydroxylase. Moreover, analysis of non-structural
carbohydrate-related genes revealed that
ethylene strongly downregulated the expression of the Kunitz-type
invertase inhibitor, already known to be involved in cold-induced sweetening. All these
ethylene-induced effects were negated by
1-MCP with one notable exception:
1-MCP enhanced the sprout suppressing effect of
ethylene whilst preventing
ethylene-induced sweetening. This study supports the conclusions that: i) tubers adapt to
ethylene by regulating conserved pathways (e.g. ABA catabolism); ii)
ethylene-induced sweetening acts independently from sprout suppression, and is similar to cold-induced
sugar accumulation.