|VALDEZ, EDWARD - Retired ARS Employee|
|TUDOR, ERIN - Former ARS Employee|
|TORRES, CAROLINA - Washington State University|
Submitted to: American Society of Horticulture Science Meeting
Publication Type: Abstract Only
Publication Acceptance Date: 4/29/2021
Publication Date: 8/8/2021
Citation: McTavish, C.K., Valdez, E.L., Tudor, E.M., Torres, C., Mattheis, J.P., Rudell Jr, D.R. 2021. Triggering and eliminating sun-related apple peel browning occurring during cold storage using heat [abstract]. American Society of Horticulture Science Meeting. Paper No. 35963.
Technical Abstract: The warm, sunny summer weather that is critical for producing the highest quality apple fruit also is a principal source of loss, even in the cold chain. Sunscald is a sun-related storage disorder with symptoms of superficial peel discoloration sometimes developing after months of cold storage. Disorder development is purportedly irreversible once the temperature event in the orchard that triggers it has occurred. Most evidence to date indicates that sunscald is caused by a combination of wavelengths including infrared. We heated apple peel on the sun facing and shaded side of ‘Granny Smith’ apples to 52 °C for 3 min up to 1 month prior to harvest with the expectation of inducing sunscald. Like sunscald, injury was not present at harvest but began to develop during air storage on a similar timeline to sunscald that also developed on untreated apples. Symptoms were similar to sunscald, appearing dark brown and very superficial although more condensed than sunscald. In some instances, the two injuries coincide, and a barrier of asymptomatic peel occurred between sunscald and heat treatment symptoms. The metabolic profile of peel with the two symptoms, the barrier between the symptoms, the periphery of each symptom, sun exposed, and shaded peel were compared. This included polar, non-polar, and hydrolyzed cutin components. Peel from each condition was distinguishable based on differences in multiple metabolic pathways. Elevated levels of metabolites linked with sun exposure were also associated with sunscald while heat related metabolic change was less obvious given prior evidence. The barrier around and between the injuries had elevated levels of metabolites more associated with wound response such as 1-aminocyclopropane-1-carboxylic acid and diacylglycerides suggesting active wound response in this narrow region. These results indicate that sunscald can be mitigated by a heat event, even after the event causing the injury, by triggering a wound response that reduces or eliminates sunscald development.