Publication: Pseudomonas aeruginosa IscR-regulated ferredoxin NADP(+) reductase gene (fprB) functions in iron-sulfur cluster biogenesis and multiple stress response
Issued Date
2015-07-31
Resource Type
ISSN
19326203
Other identifier(s)
2-s2.0-84941925299
Rights
Mahidol University
Rights Holder(s)
SCOPUS
Bibliographic Citation
PLoS ONE. Vol.10, No.7 (2015)
Suggested Citation
Adisak Romsang, Jintana Duang-nkern, Wilaiwan Wirathorn, Paiboon Vattanaviboon, Skorn Mongkolsuk Pseudomonas aeruginosa IscR-regulated ferredoxin NADP(+) reductase gene (fprB) functions in iron-sulfur cluster biogenesis and multiple stress response. PLoS ONE. Vol.10, No.7 (2015). doi:10.1371/journal.pone.0134374 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/35126
Research Projects
Organizational Units
Authors
Journal Issue
Thesis
Title
Pseudomonas aeruginosa IscR-regulated ferredoxin NADP(+) reductase gene (fprB) functions in iron-sulfur cluster biogenesis and multiple stress response
Abstract
© 2015 Romsang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. 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.