PpERF17 alleviates peach fruit postharvest chilling injury under elevated CO2 by activating jasmonic acid and γ-aminobutyric acid biosynthesis

Abstract

Internal browning (IB) is a common chilling injury (CI) feature in peach fruit after prolonged cold storage. Our previous study demonstrated that low O2 and elevated CO2 (eCO2) condition of modified atmosphere (MA) storage alleviated CI by facilitating the accumulation of jasmonic acids (JAs) and γ-aminobutyric acid (GABA) in ‘Zhonghuashoutao’ (‘ZHST’) peach fruit. Here we show that 10 % CO2 alone can improve cold tolerance, with ethylene response factor 17 (PpERF17) identified as a pivotal transcription factor (TF) that promotes biosynthesis of JAs and GABA. Stable transformation of PpERF17 in tobacco resulted in reduced cold damage, attributed to decreased levels of hydrogen peroxide (H2O2) and malondialdehyde (MDA), as well as enhanced accumulation of JAs and GABA. Moreover, under eCO2, PpMYC2.1, the master regulator of JA signaling, was found to activate transcription of 13S-lipoxygenase (Pp13S-LOX), allene oxide synthase (PpAOS), 12-oxophytodienoate reductase 3 (PpOPR3) and glutamate decarboxylase (PpGAD), while also inducing the expression of the upstream TF PpERF17, thereby establishing positive feedback loops upregulating JA and GABA biosynthesis. Finally, application of methyl jasmonate (MeJA) to fruit before shelf transfer from cold storage alleviated chilling injury development, due to increased accumulation of JAs and GABA as a result of raised expression of related biosynthetic genes. Collectively, our results suggest that eCO2-induced PpERF17 enhances JAs and GABA accumulation while activating the JA signaling pathway. This contributes to a positive feedback loop mediated by PpMYC2.1, ultimately alleviating CI of peach fruit through the sustained accumulation of JAs and GABA.