Salicylic acid treatment delays apricot (Prunus armeniaca L.) fruit softening by inhibiting ethylene biosynthesis and cell wall degradation

Apricots softening senescence is a complex metabolic network, and these metabolic pathways coordinate with each other to make aging irreversible. To identify and implement treatments to delay ripening senescence in apricots, the effects of salicylic acid (SA) treatment on ethylene biosynthesis and cell wall degradation were investigated during 35 days of storage at 4 & nbsp;C and 90%-95% relative humidity. In contrast with control, SA treatment suppressed ethylene production due to inhibited ACC synthase (ACS) and ACC oxidase (ACO) activities and reduced 1-aminocyclopropane-1-carboxylic acid (ACC) content. Furthermore, the decreases in fruit firmness, contents of CDTA-soluble pectin (CSP), Na2CO3-soluble pectin (NSP), hemicellulose as well as cellulose, and the increase in water-soluble pectin (WSP) of the apricots could be delayed by SA treatment. Enzyme activities of cellulase (EC 3.2.1.4), beta-glucosidase (EC 3.2.1.21), polygalacturonase (PG; EC 3.2.1.15), pectin methylesterase (PME; EC 3.1.1.11) as well as PaPG1 and PaPME1 gene expressions were suppressed strongly by SA treatment and these two genes were closely correlated with fruit softening. In addition, transmission electron microscopy (TEM) images demonstrated that the softening process of SA-treated apricots could be delayed efficiently and preventing structural breakdown. These results suggest that cell wall degrading enzyme activities are regulated by ethylene, and SA treatment mitigated apricots softening by inhibiting ethylene biosynthesis and decreasing cell degrading enzyme activities.

Automated summary

Salicylic acid treatment can delay the softening process of apricots by inhibiting ethylene biosynthesis and decreasing cell wall degrading enzyme activities.