Abstract
Cold storage of fruit may induce the physiological disorder chilling injury (CI); however, the molecular basis of CI development remains largely unexplored. Simulated conditions of CI priming and suppression provided an interesting experimental system to study cold response in fruit. Peaches (cv. June Gold) at the commercial harvest (CH) or tree-ripe (TR) stages were immediately exposed to cold treatment (40 d, 0 °C) and an additional group of CH fruits were pre-conditioned 48 h at 20 °C prior to low-temperature exposure (pre-conditioning, PC). Following cold treatment, the ripening behaviour of the three groups of fruits was analysed (3 d, 20 °C). Parallel proteomic, metabolomic and targeted transcription comparisons were employed to characterize the response of fruit to CI expression. Physiological data indicated that PC suppressed CI symptoms and induced more ethylene biosynthesis than the other treatments. Differences in the protein and metabolic profiles were identified, both among treatments and before and after cold exposure. Transcriptional expression patterns of several genes were consistent with their protein abundance models. Interestingly, metabolomic and gene expression results revealed a possible role for valine and/or isoleucine in CI tolerance. Overall, this study provides new insights into molecular changes during fruit acclimation to cold environment.
Highlights
Cold is one of several important environmental stresses influencing plant performance and distribution[1]
To gain insight into the regulation of chilling injury (CI) syndrome in peach fruit during post-cold ripening at 20 °C, we examined different harvest maturities and the effect of pre-conditioning before chilling (CH, TR, and PC) for how they affect the CI responses of peach fruit after 40 d cold exposure (Fig. 1)
Controlled delayed cooling of peach fruit for two days after commercial harvest (PC) provided significant protection from CI development: PC fruit were CI-free after three days ripening at 20 °C following 40 d cold treatment
Summary
Cold is one of several important environmental stresses influencing plant performance and distribution[1]. Tolerance to low but non-freezing temperatures, a phenomenon known as cold acclimation, is a highly dynamic stress-response mechanism that involves complex cross-talk between signal transduction and gene expression[2]. Studies using microarray and RNA-Seq analysis identified numerous cold-regulated genes in peach, including AGAMOUS-LIKE, MYB transcription factor and ALCATRAZ/SPATULA transcription factor[9, 10]. Proteomic evidence corroborates these studies by identifying peach proteins involved in cold responses, such as abscisic acid stress ripening protein, type II SK2 dehydrin, PR-1 protein and voltage-dependent anion channel We hypothesize that a controlled delayed cooling (pre-conditioning) treatment just after harvest[15] serves as a priming-dependent signaling to prepare fruit against cold stresses-induced CI symptoms. Metabolomic and transcriptomic approaches before and after chilling exposure, several cold-affected proteins, metabolites, genes and pathways were identified and their involvement in peach fruit acclimation to cold is discussed
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