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Watermelon Fusarium wilt, caused by Fusarium oxysporum f. sp. niveum (FON), is one of the most important diseases, and has become a major limiting factor to watermelon production worldwide. Previous research has found that the improved biocontrol agent, F1-35, had a high control efficiency to watermelon Fusarium wilt. In this study, the control efficiency of F1-35 to watermelon Fusarium wilt was firstly tested, and the control efficiency was 61.7%. Then, we investigated the mode of action of F1-35 in controlling watermelon Fusarium wilt. Using a pairing assay, we found that F1-35 did not inhibit the normal growth of FON. To know more about the interaction between F1-35 and watermelon root, the protein expressions of roots after 12, 24, and 48 h post-inoculation were examined. A total of 1109 differentially expressed proteins were obtained. KEGG analysis found that the most differentially expressed proteins occurred in alpha-linolenic acid metabolism, cysteine and methionine metabolism, plant-pathogen interaction, and the MAPK signaling pathway to the plant. A further analysis of differentially expressed proteins showed that F1-35 triggered the jasmonic acid and ethylene pathways in watermelon. To validate our results, the qRT-PCR was used to analyze the gene expression levels of PAL , LOX1 , and CTR1 . The gene expression results showed that those genes, which were positive correlated with the JA pathway, were up-expressed, including PAL and LOX1 , and the negative associated gene, CTR1 , was down-expressed. In conclusion, the improved biocontrol agent, F1-35, improves the resistance of watermelons to FON by triggering the JA and ET pathways.

The Improved Biocontrol Agent, F1-35, Protects Watermelon against Fusarium Wilt by Triggering Jasmonic Acid and Ethylene Pathways