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An integrated metabolomic and gene expression analysis identifies heat and calcium metabolic networks underlying postharvest sweet cherry fruit senescence

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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.

Abstract

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.

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Acknowledgements

MM is grateful to the Hellenic Foundation for Research and Innovation (ELIDEK) for a PhD scholarship during this work. Partially funding was obtained from ADP 2011–2018 project funded by the Autonomous Province of Trento.

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Correspondence to Athanassios Molassiotis.

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Suppl. Fig. S1

Weight loss of sweet cherries ‘Lapins’ at 1 days at 20 ℃ after immersion in CaCl2 (0, 1, 2, and 4% CaCl2·2H2O), at three different solution temperatures (20, 40, and 50 °C) and for 2 treatment durations (5 and 10 min). Each value represents the mean of five replications per ten fruits and vertical bars represent the least significance difference (LSD), P ≤ 0.05. Red arrows indicate the treatments that were selected for conducting the final experiment (PPTX 45 kb)

Suppl. Table S1

Primary polar metabolites quantification (XLSX 45 kb)

Suppl. Table S2

Secondary metabolites quantification (XLSX 28 kb)

Suppl. Table S3

Molecular properties of primary and secondary metabolites (XLSX 37 kb)

Suppl. Table S4

Transcripts properties and primer sequence (XLSX 23 kb)

Suppl. Table S5

Relative abundance of transcripts (XLSX 21 kb)

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Michailidis, M., Karagiannis, E., Tanou, G. et al. An integrated metabolomic and gene expression analysis identifies heat and calcium metabolic networks underlying postharvest sweet cherry fruit senescence. Planta 250, 2009–2022 (2019). https://doi.org/10.1007/s00425-019-03272-6

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  • DOI: https://doi.org/10.1007/s00425-019-03272-6

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