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

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 ß-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.

PpMYB1 and PpNPR1 interact to enhance the resistance of peach fruit to Rhizopus stolonifer infection.

MYB transcription factors play important role in stress-resistance of plants. Nevertheless, the function of MYB TFs in peach Rhizopus rot remains poorly understood. Herein, Pichia guilliermondii treatment activated resistance against Rhizopus stolonifer, as illustrated by reductions in the incidence rate and severity of Rhizopus rot disease, increased enzyme activities and gene expression of chitinase (CHI) and ß-1,3-glucanase (GLU), and enhancement of energy production by inducing the activities and expression of H+-ATPase and Ca2+-ATPase, succinate dehydrogenase (SDH), and cytochrome c oxidase (CCO). Moreover, an R1-type MYB, PpMYB1, from peach fruit was induced during R. stolonifer infection and in response to P. guilliermondii treatment. PpMYB1 activated the transcription of PpCHI-EP3 and PpGLU-like genes and the energy metabolism-related gene PpH+-ATPase1 by directly targeting the MBS element. Importantly, PpMYB1 interacted with PpNPR1 to form a heterodimer, which was conducive to enhancing the activation of target gene transcription. Collectively, our findings suggest that PpMYB1 cooperates with PpNPR1 to positively regulate disease resistance by activating the disease defense system and energy metabolism in peaches.

Inhibitory Effect of Moriniafungin Produced by Setosphaeria rostrata F3736 on the Development of Rhizopus Rot.

Rhizopus rot is a serious postharvest disease of various crops caused by Rhizopus spp. and controlled mainly by synthetic fungicides. We detected the antifungal activity of a culture extract of Setosphaeria rostrata F3736 against Rhizopus oryzae. The active ingredient was identified as moriniafungin, a known sordarin derivative, which showed minimum inhibitory concentrations of 1-8 µg/ml against Colletotrichum spp. and 0.03-0.13 µg/ml against Rhizopus spp. in vitro. Moriniafungin showed protective control efficacies against Rhizopus rot on apple and peach fruits. Treatment with 25 µg/ml moriniafungin delimited the lesion diameter significantly by 100% on R. oryzae-inoculated apple fruits compared with the non-treated control. Treatment with 0.04 µg/ml of moriniafungin reduced the lesion diameter significantly by 56.45%, and treatment with higher concentrations of 0.2-25 µg/ml reduced the lesion diameter by 70-90% on Rhizopus stolonifer var. stolonifer-inoculated peach fruit. These results suggest moriniafungin has potential as a control agent of postharvest diseases caused by Rhizopus spp.

Combination of Hot Water and Ethanol to Control Postharvest Decay of Peaches and Nectarines.

Spores of Monilinia fructicola or Rhizopus stolonifer were immersed in water or 10% ethanol (EtOH) for 1, 2, 4, or 8 min at temperatures of 46 or 50°C to determine exposure times that would produce 95% lethality (LT95). EtOH reduced the LT95 by about 90%. Peaches and nectarines infected with M. fructicola were immersed in hot water alone or with EtOH to control decay. EtOH significantly increased the control of brown rot compared to water alone. Immersion of fruit in water at 46 or 50°C for 2.5 min reduced the incidence of decayed fruit from 82.8% to 59.3 and 38.8%, respectively. Immersion of fruit in 10% ethanol at 46 or 50°C for 2.5 min further reduced decay to 33.8 and 24.5%, respectively. Decay after triforine (1,000 µg ml-1) treatment was 32.8%. Two treatments, 10% EtOH at 50°C for 2.5 min and 20% EtOH at 46°C for 1.25 min, were selected for extensive evaluation. The flesh of EtOH-treated fruit was significantly firmer, approximately 4.4 N force, than that of control fruit among seven of nine cultivars evaluated. No other factor evaluated was significantly influenced by heated EtOH treatments. The EtOH content of fruit treated with 10 or 20% EtOH was approximately 520 and 100 µg g-1 1 day and 14 days after treatment, respectively.