Activation of the BABA‐induced priming defence through redox homeostasis and the modules of TGA1 and MAPKK5 in postharvest peach fruit

The priming of defence responses in pathogen‐challenged model plants undergoes a preparation phase and an expression phase for defence function. However, the priming response in postharvest fruits has not been elucidated. Here, we found that 50 mM β‐aminobutyric acid (BABA) treatment could induce two distinct pathways linked with TGA1‐related systemic acquired resistance (SAR), resulting in the alleviation of Rhizopus rot in postharvest peach fruit. The first priming phase was elicited by BABA alone, leading to the enhanced transcription of redox‐regulated genes and posttranslational modification of PpTGA1. The second phase was activated by an H2O2 burst via up‐regulation of PpRBOH genes and stimulation of the MAPK cascade on pathogen invasion, resulting in a robust defence. In the MAPK cascade, PpMAPKK5 was identified as a shortcut interacting protein of PpTGA1 and increased the DNA binding activity of PpTGA1 for the activation of salicylic acid (SA)‐responsive PR genes. The overexpression of PpMAPKK5 in Arabidopsis caused the constitutive transcription of SA‐dependent PR genes and as a result conferred resistance against the fungus Rhizopus stolonifer. Hence, we suggest that the BABA‐induced priming defence in peaches is activated by redox homeostasis with an elicitor‐induced reductive signalling and a pathogen‐stimulated H2O2 burst, which is accompanied by the possible phosphorylation of PpTGA1 by PpMAPKK5 for signal amplification.
BABA elicitation regulates the redox homeostasis and shortcut interaction of TGA1 and MAPKK5 for a SAR‐related priming defence in postharvest peaches.