β-Aminobutyric acid-induced resistance in postharvest peach fruit involves interaction between the MAPK cascade and SNARE13 protein in the salicylic acid-dependent pathway.

This article focuses on elucidating the mitogen-activated protein kinase (MAPK) cascade involved in β-aminobutyric acid (BABA)-induced resistance (BABA-IR) against the fungal pathogen Rhizopus stolonifer in postharvest peach (Prunus persica) fruit. The study identifies a complete MAPK cascade composed of PpMAPKKK3, PpMAPKK5, and PpMAPK1 that is activated by BABA treatment, leading to enhanced pattern-triggered immunity (PTI), reactive oxygen species (ROS) accumulation, and salicylic acid (SA)-dependent defense gene expression. Downstream of this cascade, the SNARE13 protein interacts with PpMAPK1 and the NONEXPRESSOR OF PATHOGENESIS-RELATED GENES 1 (NPR1) protein to regulate SA signaling and systemic acquired resistance (SAR). Functional analyses using CRISPR/Cas9-generated mutants and overexpression lines in peach and Arabidopsis demonstrate that disruption of any component of this cascade or SNARE13 compromises BABA-elicited resistance, while overexpression enhances fungal resistance through SA-mediated pathways. These findings reveal a signaling module linking BABA-induced MAPK activation to vesicle trafficking and SA-dependent defense, advancing understanding of priming defense mechanisms in postharvest fruit.