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Efficient and economical iron metabolism of Aspergillus fumigatus protects its mitochondria in the absence of Mn-superoxide dismutase

ABSTRACT: The importance of manganese superoxide dismutase (Mn-SOD), an evolutionarily ancient metalloenzyme maintaining the integrity and functions of mitochondria, was studied in oxidative stress treated Aspergillus fumigatus cultures. Deletion of the Mn-SOD gene (sodB) increased both the menadione sodium bisulfite (MSB) elicited oxidative stress, and the deferiprone (DFP) induced iron limitation stress sensitivity of the strain. Moreover, DFP treatment enhanced the MSB sensitivity of both the gene deletion mutant and the reference strain. Concurring with these results, RNS sequencing data also demonstrated that deletion of sodB largely altered the MSB induced oxidative stress response. The difference between the oxidative stress responses of the two strains manifested mainly in the intensity of the response. Importantly, upregulation of “Ribosome protein”, “Iron uptake”, and Fe-S cluster assembly” genes, alterations in the transcription of “Fe-S cluster protein” genes, downregulation of “Heme binding protein” genes under MSB stress were characteristic for only the DsodB gene deletion mutant. We assume that the elevated superoxide level generated by MSB treatment may have destroyed Fe-S cluster proteins of mitochondria in the absence of SodB mediated protection. Re-synthesis of Fe-S cluster proteins enhanced translation and increased iron demand changing iron metabolism and increasing DFP sensitivity considerably.

ORGANISM(S): Aspergillus fumigatus

PROVIDER: GSE269970 | GEO | 2025/01/01

REPOSITORIES: GEO

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