Abstract

Potato cultivars Premier Russet, GemStar Russet, Defender and Russet Burbank differ substantially in resistance to low temperature sweetening (LTS) and associated metabolism. ‘Gemstar Russet’ and ‘Premier Russet’ have moderate and high resistances, respectively, while ‘Defender’ loses processing quality progressively during storage at 9°C, and similar to ‘Russet Burbank’, has virtually no resistance to LTS at 4°C. The different mechanisms of LTS resistance or susceptibility in these cultivars were indicated by changes in sucrose (Suc), fructose (Fru) and glucose (Glc) concentrations in relation to tuber respiratory profiles during wound healing (9°C), LTS (4°C) and reconditioning (16°C). At 4°C, ‘Premier Russet’ tubers maintained low levels of Suc and reducing sugars (RS, Glc+Fru), while ‘GemStar Russet’ tubers accumulated Suc with little inversion to RS. ‘Defender’ and ‘Russet Burbank’ tubers accumulated RS during LTS but only moderate levels of Suc. Changes in RS content reflected the combined activities of acid invertase and its endogenous inhibitor. In response to an immediate drop from 9°C to 4°C, tuber respiration decreased to a minimum and then increased to a new maximum over the next approximately 5 days, before decreasing to a constant basal rate at 4°C. Relative changes in respiration from the minimum to maximum rate during cold acclimation (respiratory acclimation response, RAR) were 80% for ‘GemStar Russet’ and ‘Defender’, 51% for ‘Russet Burbank’ and 26% for ‘Premier Russet’. The RARs correlated with total sugar (Suc+Glc+Fru) accumulation during LTS and likely reflected the metabolic energy required to catabolize starch to Suc, Glc and Fru. The relative ratio of Fru/Glc was also demonstrative of LTS-resistance, discriminating genotypes that accumulated Suc versus RS under LTS conditions. Changes in carbohydrates, invertase, respiration rates and RARs in response to temperature over the wound healing, LTS and reconditioning phases of storage characterized the LTS phenotypes unique to each cultivar, and revealed different mechanisms of resistance to LTS.

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