Defence responses in leaves of resistant and susceptible melon (Cucumis melo L.) cultivars infected with Colletotrichum lagenarium

Leaves of the susceptible melon cultivar Galaxy develop spreading necrotic lesions following inoculation with Colletotrichum lagenarium, while restricted lesions develop on the resistant cultivar Ultrasweet Miami. Lesion restriction in Ultrasweet Miami was associated with the intense and localised release of superoxide and hydrogen peroxide around the appressorium and surrounding epidermal cells within 24 h after inoculation (hai). The activity of the antioxidants superoxide dismutase and peroxidase significantly increased in both cultivars after inoculation, while levels of both peroxidase and ascorbate peroxidase activity were significantly higher in the resistant cultivar. Glutathione reductase activity increased in both cultivars up to 72 hai, but was higher in the resistant cultivar, resulting in higher levels of ascorbic acid and reduced glutathione. Within 48 hai callose deposits developed where hydrogen peroxide had previously been observed in inoculated leaves of Ultrasweet Miami, with only diffuse deposits in the susceptible cultivar, Galaxy. Phenylalanine ammonia lyase activity increased in inoculated leaves of the resistant cultivar, resulting in extensive and locally intense deposition of phenolic compounds and lignin around appressoria and surrounding epidermal cells between 48 h and 72 hai. By 48 hai higher levels of glycosylated precursors of antifungal phenolic compounds and the pathogenesis related proteins chitinase and β-1, 3-glucanase had accumulated in the resistant cultivar. These findings show that resistance of melon plants against C. lagenarium is associated with the rapid, localised and intense release of reactive oxygen, resulting in altered cellular redox status, cell wall strengthening, accumulation of antifungal phenolic compounds and pathogenesis-related proteins.