Superoxide dismutase SodB is essential for growth on non-fermentable carbon sources and conidiation under mitochondrial stress in Aspergillus nidulans.

Superoxide dismutases (SODs) play crucial roles in cellular oxidative stress defense. In Aspergillus nidulans, SodB is a mitochondria-localized SOD whose physiological function remains poorly understood. Here, we show that a ΔsodB mutant displays impaired growth on non-fermentable carbon sources including acetate, ethanol, threonine, and Tween 20/80, suggesting compromised mitochondrial function. Oxygen consumption assays using an extracellular oxygen consumption reagent revealed a ~50% reduction in respiratory activity in the ΔsodB strain compared to the wild type. When mitochondrial respiration was inhibited by Antimycin A or salicylhydroxamic acid, giant colony growth was equally suppressed across wild-type, ΔsodA, ΔsodB, and complemented strains. However, conidial production was significantly reduced in ΔsodB under Antimycin A treatment, and morphological abnormalities in conidiophore heads were observed under this condition. These results indicate that SodB is not only involved in mitochondrial respiration but also required for maintaining normal sporulation under mitochondrial stress conditions. This study provides new insights into the role of mitochondrial ROS defense systems in filamentous fungal development.