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MADS-box genes play well-documented roles in plant development, but relatively little is known regarding their involvement in defence responses. In this study, pre-treatment of peach (Prunus persica) fruit with β-aminobutyric acid (BABA) activated resistance against Rhizopus stolonifer, leading to a significant delay in the symptomatic appearance of disease. This was associated with an integrated defence response that included a H2O2 burst, ABA accumulation, and callose deposition. cDNA library screening identified nucleus-localized MADS2 as an interacting partner with NPR1, and this was further confirmed by yeast two-hybrid, luciferase complementation imaging, and co-immunoprecipitation assays. The DNA-binding activity of NPR1 conferred by the NPR1-MADS2 complex was required for the transcription of SA-dependent pathogenesis-related (PR) and ABA-inducible CalS genes in order to gain the BABA-induced resistance, in which MAPK1-induced post-translational modification of MADS2 was also involved. In accordance with this, overexpression of PpMADS2 in Arabidopsis potentiated the transcription of a group of PR genes and conferred fungal resistance in the transgenic plants. Conversely, Arabidopsis mads2-knockout lines showed high sensitivity to the fungal pathogen. Our results indicate that MADS2 positively participates in BABA-elicited defence in peach through a combination of SA-dependent NPR1 activation and ABA signaling-induced callose accumulation, and that this defence is also related to the post-translational modification of MADS2 by MAPK1 for signal amplification.

MADS2 regulates priming defence in postharvest peach through combined salicylic acid and abscisic acid signaling