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P .  aeruginosa  (PAO1) has two putative genes encoding ferredoxin NADP(+) reductases, denoted  fprA  and  fprB . Here, the regulation of  fprB  expression and the protein’s physiological roles in [4Fe-4S] cluster biogenesis and stress protection are characterized. The  fprB  mutant has defects in [4Fe-4S] cluster biogenesis, as shown by reduced activities of [4Fe-4S] cluster-containing enzymes. Inactivation of the gene resulted in increased sensitivity to oxidative, thiol, osmotic and metal stresses compared with the PAO1 wild type. The increased sensitivity could be partially or completely suppressed by high expression of genes from the  isc  operon, which are involved in [Fe-S] cluster biogenesis, indicating that stress sensitivity in the  fprB  mutant is partially caused by a reduction in levels of [4Fe-4S] clusters. The pattern and regulation of  fprB  expression are in agreement with the gene physiological roles;  fprB  expression was highly induced by redox cycling drugs and diamide and was moderately induced by peroxides, an iron chelator and salt stress. The stress-induced expression of  fprB  was abolished by a deletion of the  iscR  gene. An IscR DNA-binding site close to  fprB  promoter elements was identified and confirmed by specific binding of purified IscR. Analysis of the regulation of  fprB  expression supports the role of IscR in directly regulating  fprB  transcription as a transcription activator. The combination of IscR-regulated expression of  fprB  and the  fprB  roles in response to multiple stressors emphasizes the importance of [Fe-S] cluster homeostasis in both gene regulation and stress protection.

plos one

Pseudomonas aeruginosa IscR-Regulated Ferredoxin NADP(+) Reductase Gene (fprB) Functions in Iron-Sulfur Cluster Biogenesis and Multiple Stress Response