Molecular mechanism of PpGST3 response to salicylic acid regulating sand pear (Pyrus pyrifolia) fruit senescence

Postharvest fruit quality is governed by hormonal signaling and redox homeostasis, which collectively regulate senescence. Salicylic acid (SA) effectively delays fruit senescence. Glutathione S-transferases (GSTs) are also implicated in senescence regulation, but their functions remain unclear in sand pear. Here, a novel GST gene, PpGST3, was identified from transcriptomic analysis, which was downregulated by SA during sand pear senescence. PpGST3 is localized to the cytoplasm, and its overexpression in sand pear fruits and calli accelerated softening, oxidative damage, and cell wall degradation by suppressing antioxidant enzyme activities. In contrast, silencing delayed senescence and reduced oxidative stress. SA treatment further alleviated senescence by maintaining antioxidant capacity and lowering malondialdehyde levels. PpGST3 physically interacted with the SA-responsive transcription factor PpTGA2.1-L to form a functional complex. Promoter analyses revealed that ethylene-responsive factors (ERFs) activated PpGST3 transcription, while PpTGA2.1-L acted as a repressor, indicating SA-ethylene crosstalk. Collectively, these results indicate that PpGST3 acts as a positive regulator of fruit senescence, whereas SA antagonizes this pathway, thereby delaying post-harvest deterioration and extending fruit shelf life. • PpGST3 acts as a positive regulator of postharvest senescence in sand pear fruit. • Salicylic acid (SA) suppresses PpGST3 expression and delays fruit senescence. • Overexpression of PpGST3 accelerates softening, while silencing delays senescence. • PpGST3 is regulated by PpTGA2.1-L and PpERF transcription factors. • SA-ethylene crosstalk fine-tunes PpGST3-mediated postharvest fruit deterioration.