MADS-box genes play well-documented roles in plant development, but relatively little has been recorded regarding their involvement in the defence response. Herein, the treatment of peach fruit with BABA activated resistance against Rhizopus stolonifer, leading to a significant delay in the symptomatic appearance of Rhizopus rot disease. This protection was greatly potent in R. stolonifer-inoculated peaches and equipped the intertwined defence response containing H2O2 burst, ABA accumulation and callose deposition. Moreover, nucleus-localized PpMADS2 was identified as a PpNPR1 interacting partner via cDNA library screening. Y2H, LCI and co-IP assays further verified the interaction between PpNPR1 and PpMADS2. The DNA binding activity of PpNPR1 conferred by the PpNPR1-PpMADS2 complex was required for the transcription of SA-dependent PR and ABA-inducible PpCalS genes to gain the augmented BABA-IR, in which the PpMAPK1-induced posttranslational modification of PpMADS2 simultaneously was involved. Accordingly, PpMADS2 overexpression potentiated the transcription of a group of PR genes and fungal resistance in transgenic Arabidopsis. Conversely, mads2 knockout lines showed high sensitivity to fungal pathogen. Therefore, the results indicate that PpMADS2 positively participates in the BABA-elicited defence in peaches through the collaboration of SA-dependent NPR1 activation and ABA-signaling callose accumulation, which is also related to the posttranslational modification of PpMADS2 by PpMAPK1 for signal amplification.

The method were carefully recorded in MS.