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Fruit softening exacerbates mechanical damage incurred during shipping and handling and the increase in pathogen susceptibility. Here, oligogalacturonides (OGs) produced by fungal polygalacturonase (PG) delayed fruit softening in tomato and maintained fruit firmness at 8.37 ± 0.45 N at 13 d of storage, which was consistent with the fruit firmness level of 5 d in the control groups. From RNA sequencing data in line production of phytohormones, we confirmed ethylene and jasmonic acid signals, the MAPK signaling cascade, and calmodulin involved in the OG-mediated firmness response of whole fruit. SlPG2, SlPL3, and SlPL5were the major contributing factors for fruit softening, and their expression decreased continuously upon OG application. Suppression of the expression of ethylene response factors using a virus-induced gene-silencing strategy revealed that SlERF6was negatively involved in OG-restrained fruit softening. Taken together, these results indicated that fungal PG-generated OGs have potential application value in controlling tomato fruit softening.

Postharvest decay, primarily caused by pathogenic fungi in ripening fruits and fresh vegetables, poses a challenge to agricultural sustainability and results in significant economic losses. The regulation of the fruit ripening by DNA methylation has been well demonstrated, while defense response of fruit underlying epigenetic regulation against postharvest decay remains uncertain. In the present study, treatment of tomato fruits with the DNA methyltransferase inhibitor 5-Azacytidine (5-Aza) notably decreased their susceptibility to gray mold. Following 5-Aza treatment, we observed a substantial increase in activities of chitinase (CHI) and glucanase (GLU) in tomato fruits, as well as an increase in the expression of the dicer-like SlDCL2gene family. Suppression of SlDCL2cthrough double-stranded RNA-induced RNA interference (RNAi) resulted in a decrease in the expression of chitinases CHI3, CHI9, Class V chitinase, and endochitinase 4by 71%, 29%, 55%, 64%, as well as glucanases Cel1, Cel2, and GluBby 19%, 93%, and 87%, respectively. This was accompanied by decreased activities of resistance-related enzymes, including CHI and GLU. The expression levels of genes phenylalanine ammonia-lyase PAL2, peroxidase POD 12, POD P7, CCR1, CYP84A2, and COMTin phenylpropanoid biosynthesis pathway also decreased by 33%, 53%, 18%, 50%, 30%, and 24% in SlDCL2c-RNAi fruit, resulting in decreased activities of PAL and POD. Consequently, the lesion diameter of gray mold in SlDCL2c-RNAi fruit increased by 55% compared to the control group. Overall, the present study indicated that DNA methyltransferase inhibitor 5-Aza reduces susceptibility of tomato fruit to gray mold through regulation of DCL2c-mediated inducible defense response.

The acquisition of susceptibility to necrotrophy over the course of ripening is one of the critical factors limiting shelf life. In this study, phytopathology and molecular biology were employed to explore the roles of pectinase in fruit susceptibility and ripening. Solanum lycopersicumfruit softened dramatically from entirely green to 50% red, which was accompanied by a continuously high expressed SlPG2 gene. The necrotrophic fungus Botrytis cinereafurther activated the expression of SlPGs and SlPMEs to accelerate cell wall disassembly, while most of the polygalacturonase inhibitor proteins encoding genes expression were postponed in ripe fruit following the pathogen attack. Pectin induced the antagonistic yeast to secrete pectinolytic enzymes to increase fruit resistance against gray mold. The activities of pathogenic pectinase of B. cinereawere correspondingly depressed in the pectin-inducible yeast enzyme elicited ripe fruit. These data suggest that pectinase is a molecular target for regulation of disease resistance during fruit ripening.