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

Abstract

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.

Keywords: JA and ET pathway; biological control; proteomes; qRT-PCR; watermelon Fusarium wilt.

Figure 1

Distribution of differentially expressed proteins. (a): The up-regulated expression in watermelon response to F1-35 at 12, 24, and 48 hpi. (b): The down-regulated expression in watermelon response to F1-35 at 12, 24, and 48 hpi. T1: CK treatment at 12 hpi; T2: CK treatment at 24 hpi; T3: CK treatment at 48 hpi.

Figure 2

Gene ontology annotation. (a): CK treatment at 12 hpi; (b): CK treatment at 24 hpi; (c): CK treatment at 48 hpi. BP: biological process; MF: molecular function; CC: cellular component.

Figure 2

Gene ontology annotation. (a): CK treatment at 12 hpi; (b): CK treatment at 24 hpi; (c): CK treatment at 48 hpi. BP: biological process; MF: molecular function; CC: cellular component.

Figure 3

KEGG annotation. T1 is CK treatment at 12 hpi; T2 is CK treatment at 24 hpi; and T3 is CK treatment at 48 hpi.

Figure 4

A summary of the mechanism of F1-35 protection of watermelons against FON.

Figure 5

Target gene expression level in the roots, stems, or leaves of plants treated with F1-35 or FON.