Kiwifruit [Actinidia deliciosa (A. Chev.) C.F. Liang et A.R. Ferguson, cv. “Hayward”] is classified as climacteric fruit and the initiation of endogenous ethylene production following harvest is induced by exogenous ethylene or chilling exposure. To understand the biological basis of this “dilemma,” kiwifruit ripening responses were characterized at 20°C following treatments with exogenous ethylene (100 μL L−1, 20°C, 24 h) or/and chilling temperature (0°C, 10 days). All treatments elicited kiwifruit ripening and induced softening and endogenous ethylene biosynthesis, as determined by 1-aminocyclopropane-1-carboxylic acid (ACC) content and ACC synthase (ACS) and ACC oxidase (ACO) enzyme activities after 10 days of ripening at 20°C. Comparative proteomic analysis using two-dimensional gel electrophoresis (2DE-PAGE) and nanoscale liquid chromatography coupled to tandem mass spectrometry (nanoLC-MS/MS) revealed 81 kiwifruit proteins associated with ripening. Thirty-one kiwifruit proteins were identified as commonly regulated by the three treatments accompanied by dynamic changes of 10 proteins specific to exogenous ethylene, 2 to chilling treatment, and 12 to their combination. Ethylene and/or chilling-responsive proteins were mainly involved in disease/defense, energy, protein destination/storage, and cell structure/cell wall. Interactions between the identified proteins were demonstrated by bioinformatics analysis, allowing a more complete insight into biological pathways and molecular functions affected by ripening. The present approach provides a quantitative basis for understanding the ethylene- and chilling-induced kiwifruit ripening and climacteric fruit ripening in general.

This study demonstrates that O3-induced ripening inhibition could be reversed by SNP and provides insights into the interaction between oxidative and nitrosative signalling in climacteric fruit ripening.

Superficial scald is a major physiological disorder of apple fruit (Malus domestica Borkh.) characterized by skin browning following cold storage; however, knowledge regarding the downstream processes that modulate scald phenomenon is unclear. To gain insight into the mechanisms underlying scald resistance, ‘Granny Smith’ apples after harvest were treated with diphenylamine (DPA) or 1-methylcyclopropene (1-MCP), then cold stored (0 °C for 3 months) and subsequently were ripened at room temperature (20 °C for 8 days). Phenotypic and physiological data indicated that both chemical treatments induced scald resistance while 1-MCP inhibited the ethylene-dependent ripening. A combination of multi-omic analysis in apple skin tissue enabled characterization of potential genes, proteins and metabolites that were regulated by DPA and 1-MCP at pro-symptomatic and scald-symptomatic period. Specifically, we characterized strata of scald resistance responses, among which we focus on selected pathways including dehydroabietic acid biosynthesis and UDP-D-glucose regulation. Through this approach, we revealed scald-associated transcriptional, proteomic and metabolic signatures and identified pathways modulated by the common or distinct functions of DPA and 1-MCP. Also, evidence is presented supporting that cytosine methylation-based epigenetic regulation is involved in scald resistance. Results allow a greater comprehension of the ethylene–dependent and –independent metabolic events controlling scald resistance.

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