Abstract
BackgroundUnderstanding the mechanisms involved in climacteric fruit ripening is key to improve fruit harvest quality and postharvest performance. Kiwifruit (Actinidia deliciosa cv. ‘Hayward’) ripening involves a series of metabolic changes regulated by ethylene. Although 1-methylcyclopropene (1-MCP, inhibitor of ethylene action) or ozone (O3) exposure suppresses ethylene-related kiwifruit ripening, how these molecules interact during ripening is unknown.ResultsHarvested ‘Hayward’ kiwifruits were treated with 1-MCP and exposed to ethylene-free cold storage (0 °C, RH 95%) with ambient atmosphere (control) or atmosphere enriched with O3 (0.3 μL L− 1) for up to 6 months. Their subsequent ripening performance at 20 °C (90% RH) was characterized. Treatment with either 1-MCP or O3 inhibited endogenous ethylene biosynthesis and delayed fruit ripening at 20 °C. 1-MCP and O3 in combination severely inhibited kiwifruit ripening, significantly extending fruit storage potential. To characterize ethylene sensitivity of kiwifruit following 1-MCP and O3 treatments, fruit were exposed to exogenous ethylene (100 μL L− 1, 24 h) upon transfer to 20 °C following 4 and 6 months of cold storage. Exogenous ethylene treatment restored ethylene biosynthesis in fruit previously exposed in an O3-enriched atmosphere. Comparative proteomics analysis showed separate kiwifruit ripening responses, unraveled common 1-MCP- and O3-dependent metabolic pathways and identified specific proteins associated with these different ripening behaviors. Protein components that were differentially expressed following exogenous ethylene exposure after 1-MCP or O3 treatment were identified and their protein-protein interaction networks were determined. The expression of several kiwifruit ripening related genes, such as 1-aminocyclopropane-1-carboxylic acid oxidase (ACO1), ethylene receptor (ETR1), lipoxygenase (LOX1), geranylgeranyl diphosphate synthase (GGP1), and expansin (EXP2), was strongly affected by O3, 1-MCP, their combination, and exogenously applied ethylene.ConclusionsOur findings suggest that the combination of 1-MCP and O3 functions as a robust repressive modulator of kiwifruit ripening and provide new insight into the metabolic events underlying ethylene-induced and ethylene-independent ripening outcomes.
Highlights
Understanding the mechanisms involved in climacteric fruit ripening is key to improve fruit harvest quality and postharvest performance
To clarify whether the inhibition of endogenous ethylene production observed in kiwifruit exposed to O3 and 1-MCP could be recovered by a short treatment with exogenous ethylene, an intermittent experiment was set up
27.6 μL kg h− 1) after 14 or 8 d ripening in response to exogenous ethylene exposure following 4 or 6 months of cold storage, respectively (Fig. 2a, c). 1-MCP-treated fruit stored without O3 exhibited onset of ethylene production
Summary
Understanding the mechanisms involved in climacteric fruit ripening is key to improve fruit harvest quality and postharvest performance. Pre-climacteric exposure to 1-methylcyclopropene (1-MCP), through its high affinity for binding to ethylene receptors can inhibit the perception of ethylene in fruit tissues [5], delay ethylene-dependent ripening and senescence and prolong fruit storage life [6, 7]. 1-MCP inhibits kiwifruit softening by reducing cell wall related gene expression, such as polygalacturonase (PG) and expansin (EXP) [10,11,12].
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