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Abstract

Fusarium verticillioides is a mycotoxigenic pathogen of corn, capable of an intimate host association via asymptomatic endophytism and seed infection. Through production of fumonisin mycotoxins, this fungus threatens the industrial and agricultural uses of maize grain. Fumonisin consumption causes lethal diseases in livestock and is linked to esophageal cancers in humans, leading to mandatory regulation. The ubiquity of this pathogen and its close association with the host pose a significant challenge to chemical control strategies, presenting an opportunity for efficacious biological control. The work detailed here characterizes the interaction of F. verticillioides with a bacterial endophyte of maize and potential biocontrol agent, Bacillus mojavensis strain RRC101. Initial work resulted in the sequencing and annotation of the RRC101 genome for biocontrol-relevant genes, identifying synthetase operons for surfactin and fengycin class lipopeptides. Further work identified the fengycins as primary antifungal secondary metabolites involved in antagonism of F. verticillioides. This antagonism generates severe hyphal deformation and lysis, accompanied by increased secondary metabolic activity. Subsequent analysis focused on evaluating the specificity of F. verticillioides response to lipopeptide challenge, through transcriptomic analysis of cultures exposed to individual classes and synergistic antagonism. Bioinformatic characterization of lipopeptide-responsive genes identified differential localization and functional enrichment across lipopeptide classes, suggesting nuanced perception of antagonism in F. verticillioides. These transcriptomic data revealed that antagonism induces putative core stress response genes, as well as those involved in maize colonization, indicating common stress pathways involved in microbial antagonism and maize colonization. Additionally, microscopic and biochemical phenotypes of antagonism were corroborated as genes involved in structural components and secondary metabolism were upregulated under antagonistic conditions. These data also provided support for apoptosis-induction as a consequence of lipopeptide antagonism, suggesting an additional mechanism of action underlying this biological control. Together, these data illustrate the differential response of F. verticillioides to bacterial lipopeptides and characterize the subsequent response of this phytopathogen to antagonistic conditions.

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