Fig. 5
Pictorial representation of a presumptive multifaceted model of disease resistance mechanisms in Fusarium wilt-resistant watermelon varieties against Fusarium oxysporum F. sp. niveum (FON) pathogen. In Fusarium wilt-resistant watermelon varieties, Me-JA and JA-Ile accumulated upon infection and may provide induced resistance by the increased biosynthesis of defense enzymes and phytoalexins, including lowering of ROS. Conversely, high endogenous melatonin content of resistant watermelon varieties and/or formation of its catabolized metabolites such as 2-hydroxymelatonin (2HOM), cyclic-3-hydroxymelatonin (C3HOM), and N1-acetyl-N2-formyl-5-methoxyknuramine (AFMK) may develop added resistance in resistant varieties upon FON 0 infection. Similarly, pipecilic acid, a catabolic product of lysine, may further boost induced resistance in watermelon varieties