Global Transcriptomic Changes Elicited by sodB Deletion and Menadione Exposure in Aspergillus nidulans

Manganese superoxide dismutases (MnSODs) play a pivotal role in the preservation of mitochondrial integrity and function in fungi under various endogenous and exogenous stresses. Deletion of Aspergillus nidulans mnSOD/SodB increased oxidative stress sensitivity and apoptotic cell death rates as well as affected antioxidant enzyme and sterigmatocystin productions, respiration, conidiation and the stress tolerance of conidiospores. The physiological consequences of the lack of sodB were more pronounced during carbon starvation than in the presence of glucose. Lack of SodB also affected the changes in the transcriptome, recorded by high-throughput RNA sequencing, in menadione sodium bisulfite (MSB)-exposed, submerged cultures supplemented with glucose. Surprisingly, the difference between the global transcriptional changes of the Delta sodB mutant and the control strain were relatively small, indicating that the SodB-dependent maintenance of mitochondrial integrity was not essential under these experimental conditions. Owing to the outstanding physiological flexibility of the Aspergilli, certain antioxidant enzymes and endogenous antioxidants together with the reduction in mitochondrial functions compensated well for the lack of SodB. The lack of sodB reduced the growth of surface cultures more than of the submerged culture, which should be considered in future development of fungal disinfection methods.

Automated summary

Manganese superoxide dismutases (MnSODs) play a crucial role in preserving the integrity and function of mitochondria in fungi. The lack of MnSOD can lead to increased oxidative stress sensitivity, cell death rates, and affect various physiological processes and the production of antioxidant enzymes. However, under specific experimental conditions, other antioxidant enzymes and endogenous antioxidants can compensate for the absence of MnSOD to some extent.