Chemical induction of DNA demethylation by 5-Azacytidine enhances tomato fruit defense against gray mold through dicer-like protein .

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.

Dextran as an elicitor of phenylpropanoid and flavonoid biosynthesis in tomato fruit against gray mold infection.

Alpha-1,3-glucan is often synthesized on the surface of pathogenic filamentous fungi cell walls to block pathogen-associated molecular patterns (PAMPs) generation by host plant enzymes and the subsequent immune system response of the plant. Here, Botrytis cinerea susceptibility was assessed in tomato fruit to determine whether the fruit could recognize this camouflage and mount an immune response to it. The results showed that local mechanical wounds treated with dextran and laminarin, except amylopectin, could locally and then systemically activate disease resistance against B.