Abstract
Polyamines are growth regulators that have been widely implicated in abiotic and biotic stresses. They are also associated with fruit set, ripening, and regulation of fruit quality-related traits. Modulation of their content confers fruit resilience, with polyamine application generally inhibiting postharvest decay. Changes in the content of free and conjugated polyamines in response to stress are highly dependent on the type of abiotic stress applied or the lifestyle of the pathogen. Recent studies suggest that exogenous application of polyamines or modulation of polyamine content by gene editing can confer tolerance to multiple abiotic and biotic stresses simultaneously. In this review, we explore data on polyamine synthesis and catabolism in fruit related to pre- and postharvest stresses. Studies of mutant plants, priming of stress responses, and treatments with polyamines and polyamine inhibitors indicate that these growth regulators can be manipulated to increase fruit productivity with reduced use of pesticides and therefore, under more sustainable conditions.
Highlights
Polyamines (PAs) are small aliphatic amines that regulate various cellular functions
Several publications have suggested that the role played by these growth regulators in plant–microbe interactions is either exerted directly by PAs functioning as signaling molecules or mediated through the products of their catabolism together with jasmonic acid (JA), abscisic acid (ABA), salicylic acid (SA), auxins, cytokinins, and ethylene (Jiménez-Bremont et al, 2014)
Many of the studies conducted to date have indicated that PA synthesis, conjugation, and catabolism play important roles in abiotic and biotic stress responses in fruit
Summary
Polyamines (PAs) are small aliphatic amines that regulate various cellular functions. The gene encoding arginase was downregulated in response to several abiotic stresses in tomato, suggesting that synthesis of PAs occurs preferentially through ADC. Changes in PA metabolism in response to biotic stress seem to involve mainly inhibition of PA catabolism via downregulation of genes encoding CuAO and PAO.
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