Effects of acetylsalicylic acid on kiwifruit ethylene biosynthesis and signaling components

•Acetylsalicylic acid (ASA) treatment inhibited ethylene production in both whole kiwifruit and fruit flesh discs.•Combination ASA/ethylene treatments had different inhibitory effects on fruit ripening, with ASA + C2H4 relatively more effective than C2H4 + ASA.•ASA blocked ethylene perception, by inhibiting ethylene-induced expression of ethylene receptor genes (AdETR1, AdETR2, AdETR3, AdERS1a).•Softening-related ethylene signaling components were generally non-responsive to ASA treatment.•Ethylene response genes, AdERF1, AdERF3 and AdERF12, were ASA responsive.

The effects of acetylsalicylic acid (ASA) on kiwifruit (Actinidia deliciosa cvs Bruno and Hayward) ethylene biosynthesis and signaling were investigated. Exogenous application of ASA inhibited ethylene production in both whole fruit, and in vitro with flesh discs, and enzymes associated with ethylene biosynthesis (ACS and ACO). The effect of ASA treatment on kiwifruit softening was relatively weak. Combination treatments also had inhibitory effects on fruit ripening, with ASA + C2H4 more effective than C2H4 + ASA. In order to evaluate the effects of ASA on ethylene signaling, twenty-four ethylene signaling components (five ethylene receptors, two CTR1 like genes, four EIN3-like genes and thirteen ERF genes) were analyzed at the transcriptional level. The results indicated that ASA treatment generally inhibited ethylene-induced modulation of ethylene receptor genes, and had little effect on softening-related ethylene signaling components, which suggested that ASA inhibits fruit ripening mainly by interfering directly with ethylene biosynthesis and perception. In addition, the ethylene response factors AdERF1, AdERF3 and AdERF12 were characterized as ASA-responsive genes, and their roles in fruit stress response are also discussed.