Phytosulfokine α (PSKα) treatment enhances chilling tolerance of loquat fruit by regulating endogenous PSKα biosynthesis and energy supply via the EjPSKR1‑EjGATA18 module

Owing to low‑temperature sensitivity, loquat fruit readily develops chilling injury (CI) under cold stress. Although earlier studies have demonstrated that phytosulfokine α (PSKα) treatment alleviated CI in loquat fruit, whether this involves energy metabolism regulation and how PSKα signaling is involved remain unclear. In this study, the mechanisms underlying exogenous PSKα‑induced endogenous PSKα accumulation and energy supply were investigated and the role of the EjPSKR1‑EjGATA18 module in this process was revealed. PSKα treatment ensured sufficient energy supply by upregulating gene expression and enhancing enzyme activities related to energy metabolism, including H + -ATPase, Ca 2+ -ATPase, succinate dehydrogenase (SDH), and cytochrome c oxidase (CCO), thereby contributing to the improvement of cold tolerance. Meanwhile, PSKα treatment upregulated the expression of PSKα synthesis‑related genes ( EjPSK4 and EjTPST‑like ) to promote PSKα biosynthesis and trigger endogenous PSKα signaling. EjGATA18, a PSKα‑induced transcription factor with transcriptional activation activity, was identified to bind and activate the EjH + -ATPase4 , EjCa 2+ -ATPase12 , EjPSK4 , and EjTPST-like promoters. Furthermore, PSKα-upregulated EjPSKR1 was found to interact with EjGATA18 and potentiate its transcriptional activation of these target genes. Collectively, these findings indicated that PSKα treatment triggered endogenous PSKα signaling and maintained elevated energy levels by enhancing the EjPSKR1-EjGATA18 module-mediated transcriptional activation of key genes involved in PSKα biosynthesis and energy metabolism, thereby improving chilling tolerance in loquat fruit.