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

The inducer β-aminobutyric acid (BABA) participates in the immune response in various plants. However, the specific mitogen-activated protein kinase (MAPK) cascade involved in BABA-induced resistance (BABA-IR) has not yet been elucidated. Here, peach (Prunus persica) fruits treated with the BABA exhibited pattern-triggered immunity defense against Rhizopus stolonifer, accompanied by the generation of reactive oxygen species and activation of a MAPK cascade. Transcriptome sequencing suggested that a total of 15 MAPK kinase kinase (PpMAPKKK)/MAPK kinase (PpMAPKK)/PpMAPK genes were involved in BABA-IR in peach fruit. Further qRT-PCR analysis showed that the transcript profiles of PpMAPKKK3, PpMAPKK5, and PpMAPK1 were elevated. Subsequently, yeast two-hybrid, luciferase complementation imaging, pull-down, and in vitro phosphorylation assays were conducted to characterize the complete MAPK cascade (PpMAPKKK3-PpMAPKK5-PpMAPK1) involved in peach fruit. Moreover, the downstream events of MAPK1 include the involvement of SNARE13 and the corresponding NONEXPRESSOR OF PATHOGENESIS-RELATED GENES 1 (NPR1)-responsive defense. Single silencing of MAPKKK3, MAPKK5, or MAPK1 and double silencing of MAPKKK3 and MAPKK5 or MAPKK5 and MAPK1 resulted in enhanced susceptibility to the fungus R. stolonifer in mutants and attenuated salicylic acid (SA)-dependent defense gene expression. In contrast, the homologous or heterologous overexpression of PpSNARE13 in peach fruit or Arabidopsis led to an enhanced SA pool and elevated expression of pathogenesis related (PR) genes. Reciprocally, the ppsnare13cas9 mutants were generally compromised in the priming of SA-dependent resistance. Therefore, the MAPKKK3-MAPKK5-MAPK1 cascade contributed to pattern-triggered immunity signal transduction in BABA-elicited peach fruit, by combination with downstream events such as SNARE13, NPR1, and SA-dependent signaling.