Methyl jasmonate treatment regulates α-linolenic acid metabolism and jasmonate acid signaling pathway to improve chilling tolerance in both stony hard and melting flesh peaches

Peach are susceptible to chilling injury (CI) when stored at a low temperature and the postharvest application of methyl jasmonate (MeJA) is well known to alleviate CI in peach fruit. However, the optimal dose for the treatment of MeJA is still debated in peaches and the underlying mechanism remains largely unknown. In this study, we screened the optimal concentration of MeJA treatment in stony hard and melting flesh peaches, then investigated the involvement of alpha-linolenic acid metabolism and jasmonate acid (JA) signaling pathway in the MeJA-induced chilling tolerance. The results showed that 10 mol L-1 was the broad-spectrum concentration of MeJA treatment for CI alleviation in the two peach cultivars. Also, MeJA treatment improved the degree of fatty acid unsaturation in cell membrane by delaying the decrease in unsaturated fatty acids (USFAs) and the increase in saturated fatty acids (SFAs), resulting in the activation of alpha-linolenic acid metabolism. Correspondingly, it maintained a higher concentration of alpha-linolenic acid and higher activities of lipoxygenase (LOX), allene oxide synthase (AOS) and allene oxide cyclase (AOC). It also induced the expressions of PpLOX, PpAOS, PpAOC, PpACOX and PpFadA in peaches during the end of the cold storage at 5 degrees C and the shelf-life at 20 celcius. Meanwhile, the increased alpha-linolenic acid metabolism in MeJA treated fruit led to accumulations in JA and jasmonic acid isoleucine (JA-Ile), which boosted the JA signaling pathway by up-regulating the expressions of PpCOI1, PpJAZ and PpMYC2. Thus, it was suggested that MeJA treatment activated alpha-linolenic acid metabolism and JA signaling pathway might be contributing to alleviating CI in peaches during cold storage.

Automated summary

We screened the optimal concentration of MeJA treatment in peaches and found that MeJA treatment can alleviate chilling injury by activating alpha-linolenic acid metabolism and JA signaling pathway.