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.

中文翻译：

---

FvmnSOD 参与轮枝镰孢的氧化应激防御、线粒体稳定性和细胞凋亡预防

超氧化物歧化酶是消除细胞内或外源性氧化应激引发剂（如甲萘醌）产生的超氧阴离子自由基 (O2•−) 的关键酶。在这项研究中，我们通过构建基因缺失突变体 ΔFvmnSOD 并将其表型与野生型亲本菌株和 ΔFvmnSOD' C 菌株的表型进行比较，研究了锰超氧化物歧化酶编码基因在轮枝镰刀菌中的生理作用，与功能性锰超氧化物歧化酶基因相辅相成。删除 FvmnSOD 对细胞内的相对超氧化物比没有影响，但增加了真菌对 Czapek-Dox 应力琼脂平板上甲萘醌亚硫酸氢钠的敏感性。FvmnSOD 的缺乏导致线粒体形态和生理的变化：这些细胞器在第二菌丝段中的体积比，以及总的、KCN 敏感的细胞色素 c 依赖性和 KCN+SHAM（水杨酰羟胺酸）抵抗的残余呼吸率，在突变体中高于野生型和互补菌株。然而，呼吸速率的变化可归因于在基因缺失突变体中发现的线粒体体积比较高。线粒体功能的变化也带来了对由 Penicillium chrysogenum 抗真菌蛋白引起的凋亡细胞死亡的更高敏感性。与野生型菌株相比，基因缺失突变体形成了明显更薄的菌丝。FvmnSOD 的删除对在 Myro 培养基中作为静态培养物生长的真菌的伏马菌素 B1 和 B2 产生没有影响。