Abstract Green mold caused by Penicillium digitatum is a major source of postharvest loss in lemon. Here, we tested whether β-aminobutyric acid (BABA) primes lemon fruit for enhanced resistance and explored the transcriptional coordination linking redox control to antimicrobial defenses. In inoculated fruit, BABA pretreatment delayed symptom development, slowed lesion expansion, and reduced fungal biomass. Compared with inoculation alone, BABA-pretreated fruit showed attenuated H₂O₂ accumulation, lower malondialdehyde content and electrical conductivity, but higher total antioxidant capacity, indicating restrained oxidative injury. In parallel, BABA increased the accumulation of phenolics, flavonoids, and coumarins and enhanced β-1,3-glucanase and chitinase activities. In line with these coordinated defense outputs, we identified a NAC transcription factor, ClNAC72L, as a candidate regulatory node responsive to BABA priming and infection. Yeast one-hybrid assays showed that ClNAC72L binds NAC recognition sites in promoters of redox- and defense-related genes, including ClRBOHD, ClAPX, ClLOX, ClPAL, ClCHS, ClF6′H1, ClGLU, ClPR4, and ClPDF1.2. Dual-luciferase assays supported target-dependent regulation by ClNAC72L, with repression of the ClRBOHD and ClLOX promoters and activation of the other promoters tested. Consistently, transient overexpression of ClNAC72L in lemon fruit reduced disease development and fungal biomass while dampening infection-associated oxidative injury. Taken together, these results indicate that BABA primes a coordinated defense program in postharvest lemon that couples redox buffering with enhanced antimicrobial metabolism, at least in part through ClNAC72L.
Li et al. (2026) studied this question.