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Watermelon Fusarium wilt is a common soil-borne disease that has significantly affected its yield. In this study, fusaric acid-deficient mutant designated as ΔFUBT (mutated from Fusarium oxysporum f. sp. niveum, FON) was obtained. The ΔFUBT mutant showed significant decrease in fusaric acid production but maintained wild-type characteristics, such as in vitro colony morphology, size, and conidiation. A field pot experiment demonstrated that ΔFUBT could successfully colonize the rhizosphere and the roots of watermelon, leading to significant reduction in FON colonization in the watermelon plant. In addition, ΔFUBT inoculation significantly improved the rhizosphere microenvironment and effectively increased the resistance in watermelon. This study demonstrated that a nonpathogenic Fusarium mutant (ΔFUBT) could be developed as an effective microbial control agent to alleviate Fusarium wilt disease in watermelon and increase its yield.

The application of benomyl (Benlate),* methyl 1-(butyl-carbamoyl)-2-benzimidazole-carbamate, to infested soils controlled populations of the wilt Fusarium (F. oxysporum f. melonis), reduced wilt losses to low levels, and permitted a harvest to be taken. Powdery mildew (Erysiphe cichoracearum) was also inhibited. In pot culture the compound was effective in single or split applications of 0.08 g active material and in a single application of 0.16 g or 4 applications of 0.04 g each per 1000 g soil. At the above rates Benlate prevented increases in populations of the pathogen in soil planted with susceptible melons. In the field, three applications of 0.64 g each/0.09 m2 (11.49 kg/ha), or one application of either 1.28 g (7.66 kg/ha), or 2.56 g (15.32 kg/ha) controlled wilt. Treatments that controlled wilt also retarded early growth and delayed the onset of fruiting. Recovery was made, however, followed by a prolonged period of growth and fruit production.

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