FvmnSOD is involved in oxidative stress defence, mitochondrial stability and apoptosis prevention in Fusarium verticillioides

Superoxide dismutases are key enzymes in elimination of the superoxide anion radical (O2•−) generated intracellularly or by exogenous oxidative stress eliciting agents, like menadione. In this study, we investigated the physiological role of the manganese superoxide dismutase‐encoding gene in Fusarium verticillioides via the construction of a gene deletion mutant, ΔFvmnSOD and comparing its phenotype with that of the wild‐type parental strain and a ΔFvmnSOD′ C strain, complemented with the functional manganese superoxide dismutase gene. Deletion of FvmnSOD had no effect on the relative intracellular superoxide ratio but increased the sensitivity of the fungus to menadione sodium bisulphite on Czapek‐Dox stress agar plates. The lack of FvmnSOD caused changes in mitochondrial morphology and physiology: The volumetric ratio of these cell organelles in the second hyphal segment, as well as the total, the KCN‐sensitive cytochrome c‐dependent and the KCN+SHAM (salicylhidroxamic acid)‐resistant residual respiration rates, were higher in the mutant as compared to the wild‐type and the complemented strains. Nevertheless, changes in the respiration rates were attributable to the higher volumetric ratio of mitochondria found in the gene deletion mutant. Changes in the mitochondrial functions also brought about higher sensitivity to apoptotic cell death elicited by the Penicillium chrysogenum antifungal protein. The gene deletion mutant developed significantly thinner hyphae in comparison to the wild‐type strain. Deletion of FvmnSOD had no effect on fumonisin B1 and B2 production of the fungus grown in Myro medium as a static culture.