Sucrose metabolism and sensory evaluation in peach as influenced by β-aminobutyric acid (BABA)-induced disease resistance and the transcriptional mechanism involved

This study attempted to provide evidence for the inhibitory efficiency of β-aminobutyric acid (BABA) treatments on postharvest decay development, soluble sugar accumulation, and sensory profiles in peach fruit and to analyze the possible transcriptional regulation involved. Specifically, 100 mmol L−1 BABA directly induced resistance as manifested by suppression of postharvest decay progression in peaches, and this suppression was accompanied by the consistently upregulated expression of the WRKY transcription factor PpWRKY40 and a battery of pathogenesis-related (PR) genes, such as PpNPR1s, PpPR1s, PpPR2s and PpPR5s, throughout the storage period. However, treatment with 10 mmol L−1 BABA ignited priming resistance in peaches that underwent hostile conditions of high pressure during the late monitoring period. The peaches elicited by 10 mmol L−1 BABA had higher expression levels of PpSSs, PpSPSs and PpSPPs as well as lower expression levels of PpNIs and PpAIs than those treated with 100 mmol L−1 BABA, thus resulting in increases in soluble sugar content and the sweetness score during storage. On the other hand, the direct interaction between persistently highly expressed PpWRKY40 and the regulatory protein PpNPR1 was detected in vivo and in vitro by Y2H and pull-down assays; in addition, Y1H and DLR assays demonstrated that PpWRKY40 bound to the W-box motif in the promoter of sucrose-metabolizing enzyme genes, including PpSS1 and PpSPS3, and activated their transcription. Hence, we deduced that the dual regulation of key genes associated with systemic acquired resistance (SAR) and sucrose metabolism by PpWRKY40 might be conducive to the balance of fitness and defense in BABA-primed resistance by maintaining soluble sugar accumulation at an intermediate level and activating resistance against stress in harvested peaches.