|GAPPER, NIGEL - Cornell University - New York|
|HERTOG, MAARTEN - Catholic University Of Leuven|
|JOHNSTON, JASON - New Zealand Institute Of Plant & Food Research|
|SHAFFER, ROBERT - New Zealand Institute Of Plant & Food Research|
|MICOLAI, BART - Catholic University Of Leuven|
|WATKINS, CHRISTOPHER - Cornell University - New York|
Submitted to: BMC Plant Biology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 4/10/2017
Publication Date: 4/21/2017
Citation: Gapper, N.E., Hertog, M., Lee, J., Buchanan, D.A., Leisso, R.S., Giovannoni, J.J., Johnston, J.W., Shaffer, R.J., Micolai, B.M., Mattheis, J.P., Watkins, C.B., Rudell Jr, D.R. 2017. Delayed response to cold stress is characterized by successive metabolic shifts culminating in apple fruit peel necrosis. Biomed Central (BMC) Plant Biology. 17:77. https://doi.org/10.1186/s12870-017-1030-6.
Interpretive Summary: Superficial scald is an apple peel disorder that results in brown, sunken peel during long-term cold storage. The disorder results in significant economic losses to apple producers worldwide. We used untargeted profiling of metabolism to discover changes that were associated with the disorder both before and following symptom presentation. Our results revealed a number of changes of metabolite and gene expression associated potentially indicative of whether apples will develop the disorder. Most of these changes have never been reported before in apple or as a response to the chilling temperatures that provoke scald in any plant. We suggest that many of these changes can be exploited to assess the likelihood of apples developing the disorder within the supply change.
Technical Abstract: Superficial 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. The 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 a-farnesene oxidation and, later, methanol production alongside symptom development. Results 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.