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ISHS Acta Horticulturae 682: V International Postharvest Symposium

UNDERSTANDING THE BASIS OF CHILLING INJURY IN CITRUS FRUIT

Authors:   M.T. Lafuente, L. Zacarias, J.M. Sala, M.T. Sánchez-Ballesta, M.J. Gosalbes, J.F. Marcos, L. González-Candelas, Y. Lluch, A. Granell
Keywords:   membrane permeability, oxidative stress, hormones, carbohydrates, gene expression
DOI:   10.17660/ActaHortic.2005.682.108
Abstract:
Low, non-freezing, temperature is the single most important factor governing maintenance of postharvest quality in stored fruits and vegetables. It may reduce disease, control insect pest, or modify ripening processes, but it may also cause chilling injury (CI). Exposure of chilling-sensitive crops to hardening or non-lethal high temperatures may reduce injury caused by subsequent holding at chilling temperatures. Many varieties of citrus fruit are susceptible to chilling. Among them, ‘Fortune’ mandarin is a good model system to characterize metabolic events underlying CI. Considerable effort has been directed to understand the physiological and biochemical basis of low temperature tolerance in citrus fruit harvested at different maturity stages, including the role of plant hormones, alteration in lipids, carbohydrate composition, changes in phenylpropanoid metabolism and in oxidative stress-associated processes. However, we still lack solid information on the mechanisms controlling chilling. The advent of molecular technologies is providing a powerful mean for systematically evaluating the expression of large subsets of genes in response to stress cues. Studies of molecular events by which horticultural crops may tolerate chilling are in their early stages but in citrus fruit it has been shown the complexity of molecular mechanism underlying chilling tolerance. A functional categorization of genes expressed in heat-conditioned ‘Fortune’ fruit exposed to chilling has revealed that long-term heat-induced chilling tolerance is an active process, which requires expression of transcription factors, activation of secondary metabolism, and stress-related proteins, while induction of heat shock proteins (HSPs) could be ascribed to the early events of chilling acclimation. Future work is necessary to delineate the precise function of the identified chilling-associated responses, but the availability of new molecular strategies is now providing excellent tools to continue the study of the mechanism underlying chilling stress.

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