Salicylic acid delayed fruit senescence via the PpERF51B-L/PpNAC14-PpERF061- PpACO3 / PpPG1 regulatory module in sand pear

Abstract

Sand pear quality is limited by rapid postharvest senescence driven by ethylene. We identify two Ethylene Response Factors with opposing functions in this process. PpERF061 is induced by salicylic acid (SA) and repressed by the ethylene precursor ACC. Gain- and loss-of-function assays show that PpERF061 delays senescence by repressing ethylene biosynthesis and cell wall-modifying genes (PpACO3, PpPG1). PpERF061 also interacts with the NAC transcription factor PpNAC14, placing it within a broader regulatory module. In contrast, PpERF51B-L promotes senescence via two mechanisms: it forms a repressive complex with PpNAC14 to suppress PpERF061, and it engages ethylene signaling by interacting with PpEIN3a/b, with transcriptional activation by PpEIN3a. Notably, the SA receptor NPR1 attenuates PpERF51B-L’s pro-senescence activity through protein-protein interaction, revealing an SA-ethylene antagonism at the ERF node. These findings provide a mechanistic framework for manipulating hormonal crosstalk to extend shelf life and improve marketability in sand pear.