Oxidative Stress Leads to Fur‐Mediated Activation of <i>ftnA</i> in <i>Escherichia coli</i> Independently of OxyR/SoxRs Regulators

Ferritin FtnA is the main scavenger of Fe²⁺ and storage of Fe³⁺ in bacterial cells, together with Dps and Bfr it prevents the Fenton reaction. To study the regulation of Escherichia coli ftnA expression under oxidative stress conditions, we used P_ftnA-luxCDABE transcriptional fusion. It was shown that P_ftnA is induced after the addition of oxidative stress inducers. This activation was independent of the presence of functional oxyR and soxR genes in the cell, but was completely abolished in the absence of fur. The response is amplified in the ftnA mutant and is diminished in the FtnA-overproducing strain, which indicates that iron sequestration by apoferritin blocks the response and helps to cope with stress consequences. Comparison of the activation kinetics of the P_fecA and P_ftnA promoters, responsible for iron uptake and storage regulation, showed that the addition of H₂O₂ initially leads to the inactivation of Fur, causing derepression of iron uptake and, as a consequence, an increase in intracellular iron. As the redox balance in the cell is restored, Fur is reactivated, which leads to the induction of ftnA expression. Thus, oxidative stress leads to P_ftnA activation, which is mediated by Fur and time-delayed in comparison with OxyR-response.