PpMYB102 as a central regulator of pipecolic Acid-induced defense against monilinia fructicola brown rot in peach fruit

• Pipecolic acid induced the resistance to M. fructicola. • Pipecolic acid induces DEGs in hormone signaling, cell wall and defense. • Transient overexpression of PpMYB102 in peach enhanced resistance to M. fructicola. Peach fruit is highly susceptible to postharvest brown rot caused by Monilinia fructicola , leading to substantial economic losses. However, the mechanism by which exogenous pipecolic acid (Pip) enhances disease resistance remains unclear. This study examined the mechanism of exogenous Pip against brown rot in 'Okubao' peaches. Pip treatment significantly inhibited M. fructicola infection, reducing disease incidence and lesion diameter. Transcriptome analysis revealed that differentially expressed genes (DEGs) induced by Pip were primarily enriched in hormone signaling (salicylic acid, jasmonate/ethylene), cell wall metabolism, and disease resistance pathways. Temporal expression patterns indicated Pip enhances resistance through a dynamic regulatory network featuring early-stage cell wall reinforcement and hormone modulation, mid-stage disease resistance signal activation, and late-stage energy metabolism maintenance. WGCNA identified the MYB transcription factor PpMYB102 as a central Pip-induced regulator. Subcellular localization and yeast activation assays showed that PpMYB102 had nuclear localization and transcriptional activation. Transient overexpression of PpMYB102 in peach fruit significantly enhanced disease resistance by suppressing ROS accumulation, increasing antioxidant enzyme activity, and reducing membrane lipid peroxidation following M. fructicola infection. This study demonstrates that exogenous Pip enhances peach resistance to M. fructicola by inducing PpMYB102 expression to regulate antioxidant enzymes and ROS homeostasis, providing a deeper understanding of the regulatory mechanism of brown rot resistance in postharvest peach fruits.