Regulatory roles of Fnr, Fur, and Arc in expression of manganese-containing superoxide dismutase in Escherichia coli.

Abstract

Transcriptional regulation of the sodA gene, encoding the manganese superoxide dismutase (superoxide: superoxide oxidoreductase, EC 1.15.1.1) of Escherichia coli, was studied by monitoring expression of sodA-lacZ in different genetic backgrounds and under different growth conditions. Mutations in the fnr gene were found to affect aerobic and anaerobic expression of sodA-lacZ. Potential Fnr-binding sites were identified in the promoter region of sodA. Strains harboring simultaneous mutations in arcA/B and fur expressed sodA-lacZ under anaerobic growth conditions but were still inducible by iron chelators. However, in the triple mutants (fnr fur arcA/B) sodA-lacZ was fully expressed under anaerobiosis and was not further induced by the presence of 2,2'-dipyridyl, nitrate, or oxidants. On the other hand, aerobic expression of sodA-lacZ from a Fur-strain was approximately 3.8-fold higher than that from the wild-type strain but was diminished by introducing mutations in fnr or arcA/B. In conclusion, Fnr, Arc, and Fur act as anaerobic repressors of sodA. Furthermore, the regulation of sodA by Fur (ferric uptake regulation protein), Arc (aerobic respiratory control), and Fnr (fumarate nitrate reduction/regulator of anaerobic respiration) is independent of the superoxide response regulon SoxRS.