Michail Michailidis1, Evangelos Karagiannis1, Georgia Tanou2, Eirini Sarrou3, Evangelia Stavridou4, Ioannis Ganopoulos3, Katerina Karamanoli5, Panagiotis Madesis4, Stefan Martens6, Athanassios Molassiotis7. 1. Laboratory of Pomology, School of Agriculture, Aristotle University of Thessaloniki, Thermi, 57001, Thessaloniki, Greece. 2. Institute of Soil and Water Resources, ELGO-DEMETER, 57001, Thessaloníki, Greece. 3. Institute of Plant Breeding and Genetic Resources, ELGO-DEMETER, 57001, Thessaloníki, Greece. 4. Institute of Applied Biotechnology, CERTH, 57001, Thessaloníki, Greece. 5. Laboratory of Agricultural Chemistry, School of Agriculture, Aristotle University of Thessaloniki, Thessaloníki, 54124, Greece. 6. Department of Food Quality and Nutrition, Centro Ricerca E Innovazione, Fondazione Edmund Mach, San Michele All'adige, 38010, Trento, Italy. 7. Laboratory of Pomology, School of Agriculture, Aristotle University of Thessaloniki, Thermi, 57001, Thessaloniki, Greece. amolasio@agro.auth.gr.
Abstract
MAIN CONCLUSION: Ηeat and calcium treatments reprogram sweet cherry fruit metabolism during postharvest senescence as evidenced by changes in respiration, amino acid metabolism, sugars, and secondary metabolites shift. Heat and calcium treatments are used to improve postharvest fruit longevity; however, the exact mechanism remains poorly understood. To characterize the impact of these treatments on sweet cherries metabolism, 'Lapins' fruits were treated with heat or CaCl2 solutions and their combination and subsequently were exposed at room temperature, for up to 4 days, defined as senescence period. Single and combined heat and calcium treatments partially delayed fruit senescence, as evidenced by changes in fruit colour darkening, skin penetration force, and respiration activity. Calcium content was noticeably increased by heat in Ca-treated fruit. Several primary metabolites, including amino acids, organic acids, and alcohols, were decreased in response to both treatments, while many soluble sugars and secondary metabolites were increased within 1 day post-treatment. Changes of several metabolites in heat-treated fruits, especially esculetin, peonidin 3-O-glucoside and peonidin 3-O-galactoside, ribose, pyroglutamate, and isorhamnetin-3-O-rutinoside, were detected. The metabolome of fruit exposed to calcium also displayed substantial modulations, particularly in the levels of galactose, glycerate, aspartate, tryptophan, phospharate rutin, and peonidin 3-O-glucoside. The expression of several genes involved in TCA cycle (MDH1, IDH1, OGDH, SUCLA2, and SDH1-1), pectin degradation (ADPG1) as well as secondary (SK1, 4CL1, HCT, and BAN), amino acids (ALDH18A1, ALDH4A1, GS, GAD, GOT2, OPLAH, HSDH, and SDS), and sugar (PDHA1 and DLAT) metabolism were affected by both treatments. Pathway-specific analysis further revealed the regulation of fruit metabolic programming by heat and calcium. This work provides a comprehensive understanding of metabolic regulation in response to heat and calcium during fruit senescence.
MAIN CONCLUSION: Ηeat and calcium treatments reprogram sweet cherry fruit metabolism during postharvest senescence as evidenced by changes in respiration, amino acid metabolism, sugars, and secondary metabolites shift. Heat and calcium treatments are used to improve postharvest fruit longevity; however, the exact mechanism remains poorly understood. To characterize the impact of these treatments on sweet cherries metabolism, 'Lapins' fruits were treated with heat or CaCl2 solutions and their combination and subsequently were exposed at room temperature, for up to 4 days, defined as senescence period. Single and combined heat and calcium treatments partially delayed fruit senescence, as evidenced by changes in fruit colour darkening, skin penetration force, and respiration activity. Calcium content was noticeably increased by heat in Ca-treated fruit. Several primary metabolites, including amino acids, organic acids, and alcohols, were decreased in response to both treatments, while many soluble sugars and secondary metabolites were increased within 1 day post-treatment. Changes of several metabolites in heat-treated fruits, especially esculetin, peonidin 3-O-glucoside and peonidin 3-O-galactoside, ribose, pyroglutamate, and isorhamnetin-3-O-rutinoside, were detected. The metabolome of fruit exposed to calcium also displayed substantial modulations, particularly in the levels of galactose, glycerate, aspartate, tryptophan, phospharate rutin, and peonidin 3-O-glucoside. The expression of several genes involved in TCA cycle (MDH1, IDH1, OGDH, SUCLA2, and SDH1-1), pectin degradation (ADPG1) as well as secondary (SK1, 4CL1, HCT, and BAN), amino acids (ALDH18A1, ALDH4A1, GS, GAD, GOT2, OPLAH, HSDH, and SDS), and sugar (PDHA1 and DLAT) metabolism were affected by both treatments. Pathway-specific analysis further revealed the regulation of fruit metabolic programming by heat and calcium. This work provides a comprehensive understanding of metabolic regulation in response to heat and calcium during fruit senescence.