Abstract
BackgroundSuperficial scald is a physiological disorder of apple fruit characterized by sunken, necrotic lesions appearing after prolonged cold storage, although initial injury occurs much earlier in the storage period.To determine the degree to which the transition to cell death is an active process and specific metabolism involved, untargeted metabolic and transcriptomic profiling was used to follow metabolism of peel tissue over 180 d of cold storage.ResultsThe metabolome and transcriptome of peel destined to develop scald began to diverge from peel where scald was controlled using antioxidant (diphenylamine; DPA) or rendered insensitive to ethylene using 1-methylcyclopropene (1-MCP) beginning between 30 and 60 days of storage. Overall metabolic and transcriptomic shifts, representing multiple pathways and processes, occurred alongside α-farnesene oxidation and, later, methanol production alongside symptom development.ConclusionsResults indicate this form of peel necrosis is a product of an active metabolic transition involving multiple pathways triggered by chilling temperatures at cold storage inception rather than physical injury. Among multiple other pathways, enhanced methanol and methyl ester levels alongside upregulated pectin methylesterases are unique to peel that is developing scald symptoms similar to injury resulting from mechanical stress and herbivory in other plants.
Highlights
Superficial scald is a physiological disorder of apple fruit characterized by sunken, necrotic lesions appearing after prolonged cold storage, initial injury occurs much earlier in the storage period
Many of the factors that define scald, including the delay between cell damage and symptom appearance, and our evidence indicating shifting gene expression beginning with the first signs of oxidative stress of the metabolome, support the hypothesis that scald development is an active, organized process by which metabolism transitions towards cell death much as it does in the case of hypersensitive response to pathogen challenge or other established plant programmed cell death events
The culmination of symptom development provides its own very specific metabolic and transcriptional profile including a unique volatile profile containing methanol and methyl esters compared to healthy, ethylenereceptive tissue
Summary
Superficial scald is a physiological disorder of apple fruit characterized by sunken, necrotic lesions appearing after prolonged cold storage, initial injury occurs much earlier in the storage period. Application of the principal α-farnesene oxidation product, the 2,6,10-trimethyldodeca-2,7(E),9(E),11-tetraen-6-ol (CTOL) and other closely related compounds to apples at harvest resulted in symptoms visually similar to superficial scald and could be reduced in severity by prior DPA treatment [10]. Beyond this evidence and in vivo [11] and in vitro [12] CTOL level reduction with DPA treatment, little evidence links CTOL generation with ROS generating metabolism within the fruit peel suggesting the process may coincide with scald provocation rather than be directly linked with it. A 3-hydroxy-3-methylglutaryl-CoA reductase (hmgr2) [13], and α-farnesene synthase (AFS) gene expression can increase prior to or at the same time as α-farnesene production [14]
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