Ethylene –dependent and –independent superficial scald resistance mechanisms in ‘Granny Smith’ apple fruit
Authors:
- Evangelos KaragiannisEKEvangelos Karagiannis
- Michail MichailidisMichail Michailidis
- Martina SamiotakiMSMartina Samiotaki
- Katerina KaramanoliKKKaterina Karamanoli
- Evangelia AvramidouEvangelia Avramidou
- Ioannis GanopoulosIoannis Ganopoulos
- Panagiotis MadesisPanagiotis Madesis
- Athanassios MolassiotisAthanassios Molassiotis
Open Access
- 30 July 2018
- journal article
- research article
- Published by Springer Nature in Scientific Reports
- Vol. 8 (1) , 1-16
Abstract
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.Keywords
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