A PpTIFY5A/10A-PpTGA2.1-L complex delaying fruit senescence via salicylic acid antagonized ethylene and jasmonic acid in sand pear

Hormonal interactions regulate fruit senescence, but the roles of salicylic acid (SA), jasmonic acid (JA), and ethylene in sand pear remain unclear. Two SA-responsive transcription factors, PpTIFY5A and PpTIFY10A, were identified as positive regulators of fruit senescence. Both were induced by ethylene, inhibited by SA, and peaked after harvest. Subcellular localization confirmed their nuclear accumulation. Silencing PpTIFY5A / 10A delayed senescence as evidenced by maintained firmness and extended shelf life, decreased ethylene and JA, increased SA, suppressed cell wall-degrading enzymes, and alleviated oxidative stress, whereas overexpression had opposite effects. SA treatment mitigated PpTIFY-mediated senescence, maintaining firmness and redox balance. Mechanistically, PpTIFYs interacted with SA signaling protein PpTGA2.1-L and repressed PpMYC2 ; PpTIFY10A formed a complex with PpMYC2, modulating JA-responsive genes. PpMYC2 negatively regulated PpERF109-L , which activated the ethylene biosynthesis gene PpACO11 , linking JA and ethylene pathways. These results reveal an SA–TIFY–MYC2–ERF–ethylene axis controlling sand pear senescence, which provides a direct molecular target for improving practical fruit quality by delaying postharvest. • PpTIFY5A/10 A are SA-responsive positive regulators of sand pear fruit senescence. • Silencing PpTIFY5A/10 A delays senescence by modulating ethylene, JA, and SA levels. • SA delays sand pear fruit senescence via PpTGA2.1–PpTIFY5A/10 A module. • PpTIFY10A forms a complex with PpMYC2 to regulate JA signaling. • SA negatively regulates JA and ethylene biosynthesis to delay fruit senescence.