cis- and trans-acting elements involved in regulation of norB (norZ), the gene encoding nitric oxide reductase in Neisseria gonorrhoeae

Isabella, Vincent M.; Wright, Lori; Barth, Kenneth; Spence, Janice M.; Grogan, Susan; Genco, Caroline Attardo; Clark, Virginia L.

doi:10.1099/mic.0.2007/010470-0

Cited by 40 publications

(79 citation statements)

References 48 publications

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“…It is possible that Fur bound to the ompT promoter interacts directly with RNA polymerase, or it may alter the supercoiling or bending of the DNA to promote transcription. It is interesting that the putative Fur box in the ompT promoter is located in a position upstream of the Ϫ10 and Ϫ35 sites similar to that of the Fur box in N. meningitidis norB, a nitric oxide reductase gene that, like ompT, is positively regulated by iron and Fur (7,16). This suggests that Fur bound to sites upstream of the polymerase binding site allows the enhanced transcription of the gene, while Fur sites that overlap the RNA polymerase recognition site mediate the repression of gene expression.…”

Section: Discussionmentioning

confidence: 99%

Positive Regulation of the Vibrio cholerae Porin OmpT by Iron and Fur

Craig¹,

Carpenter²,

Mey³

et al. 2011

Journal of Bacteriology

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The transcription factor Fur regulates the expression of a number of genes in Vibrio cholerae in response to changes in the level of available iron. Fur usually acts as a repressor, but here we show that Fur positively regulates the expression of ompT, which encodes a major outer membrane porin. OmpT levels increased when the bacteria were grown in medium containing relatively high levels of iron, and this effect required Fur. The level of ompT mRNA also is increased in the presence of iron and Fur. The effect of iron on OmpT levels was independent of the known ompT regulators ToxR and Crp, and it did not require RyhB, which has been shown to be responsible for positive regulation by iron of some V. cholerae genes. Electrophoretic mobility shift assays showed that Fur binds upstream of the ompT transcription start site in a region overlapping known binding sites for ToxR and Crp. These data suggest that Fur and iron positively regulate ompT expression through the direct binding of Fur to the ompT promoter.

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Section: Discussionmentioning

confidence: 99%

Positive Regulation of the Vibrio cholerae Porin OmpT by Iron and Fur

Craig¹,

Carpenter²,

Mey³

et al. 2011

Journal of Bacteriology

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“…The NsrR protein, which is also predicted to contain an Fe-S center (2), represses the expression of the norB gene, but repression is lifted on exposure to low concentrations of NO (20,41). If the interpretation of the effects of a dnrN mutation on aniA expression is correct, it can be predicted that exposure to NO would result in a rapid increase in norB expression.…”

Section: Resultsmentioning

confidence: 99%

Widespread Distribution in Pathogenic Bacteria of Di-Iron Proteins That Repair Oxidative and Nitrosative Damage to Iron-Sulfur Centers

et al. 2008

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Expression of two genes of unknown function, Staphylococcus aureus scdA and Neisseria gonorrhoeae dnrN, is induced by exposure to oxidative or nitrosative stress. We show that DnrN and ScdA are di-iron proteins that protect their hosts from damage caused by exposure to nitric oxide and to hydrogen peroxide. Loss of FNR-dependent activation of aniA expression and NsrR-dependent repression of norB and dnrN expression on exposure to NO was restored in the gonococcal parent strain but not in a dnrN mutant, suggesting that DnrN is necessary for the repair of NO damage to the gonococcal transcription factors, FNR and NsrR. Restoration of aconitase activity destroyed by exposure of S. aureus to NO or H 2 O 2 required a functional scdA gene. Electron paramagnetic resonance spectra of recombinant ScdA purified from Escherichia coli confirmed the presence of a di-iron center. The recombinant scdA plasmid, but not recombinant plasmids encoding the complete Escherichia coli sufABCDSE or iscRSUAhscBAfdx operons, complemented repair defects of an E. coli ytfE mutant. Analysis of the protein sequence database revealed the importance of the two proteins based on the widespread distribution of highly conserved homologues in both gram-positive and gram-negative bacteria that are human pathogens. We provide in vivo and in vitro evidence that Fe-S clusters damaged by exposure to NO and H 2 O 2 can be repaired by this new protein family, for which we propose the name repair of iron centers, or RIC, proteins.

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“…these genes (20,28,36,50). These genes include those encoding iron-scavenging receptors and iron-regulated transporters (fbpA, hemO, tbpA, tbpB, fetB, and tonB) and genes encoding enzymes which require iron as a cofactor such as sodB (20,28,36,50).…”

Section: Discussionmentioning

confidence: 99%

“…A separate report has demonstrated that in N. gonorrhoeae Fur can function to activate transcription of the norB gene. In this case, gonococcal Fur was demonstrated to bind to the same site in the promoter region of norB as ArsR, resulting in derepression of transcription in a mechanism similar to that found in E. coli with H-NS (36). Despite these recent studies, more global knowledge of Fur-dependent activation of transcription in N. gonorrhoeae is lacking due to the absence of a defined gonococcal fur mutant.…”

mentioning

confidence: 99%

“…In Salmonella enterica serovar Typhimurium, Fur represses a repressor protein, the histone-like nucleoid structuring protein (H-NS), which negatively regulates hilA, resulting in indirect activation of hilA by Fur (52). Alternatively, other studies suggest that Fur can activate gene transcription via Fur binding to promoter regions and occluding the binding of a repressor protein, thus derepressing gene transcription (36,47). In E. coli, Fur-mediated activation of ftnA transcription is due to Fur binding to the ftnA promoter region, which results in competition for H-NS binding (47).…”

mentioning

confidence: 99%

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Fur-Mediated Activation of Gene Transcription in the Human Pathogen Neisseria gonorrhoeae

Genco

2012

J Bacteriol

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It is well established that the ferric uptake regulatory protein (Fur) functions as a transcriptional repressor in diverse microorganisms. Recent studies demonstrated that Fur also functions as a transcriptional activator. In this study we defined Fur-mediated activation of gene transcription in the sexually transmitted disease pathogen Neisseria gonorrhoeae. Analysis of 37 genes which were previously determined to be iron induced and which contained putative Fur boxes revealed that only 30 of these genes exhibited reduced transcription in a gonococcal fur mutant strain. Fur-mediated activation was established by examining binding of Fur to the putative promoter regions of 16 Fur-activated genes with variable binding affinities observed. Only ϳ50% of the newly identified Fur-regulated genes bound Fur in vitro, suggesting that additional regulatory circuits exist which may function through a Fur-mediated indirect mechanism. The gonococcal Fur-activated genes displayed variable transcription patterns in a fur mutant strain, which correlated with the position of the Fur box in each (promoter) region. These results suggest that Fur-mediated direct transcriptional activation is fulfilled by multiple mechanisms involving either competing with a repressor or recruiting RNA polymerase. Collectively, our studies have established that gonococcal Fur functions as an activator of gene transcription through both direct and indirect mechanisms.

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cis- and trans-acting elements involved in regulation of norB (norZ), the gene encoding nitric oxide reductase in Neisseria gonorrhoeae

Cited by 40 publications

References 48 publications

Positive Regulation of the Vibrio cholerae Porin OmpT by Iron and Fur

Positive Regulation of the Vibrio cholerae Porin OmpT by Iron and Fur

Widespread Distribution in Pathogenic Bacteria of Di-Iron Proteins That Repair Oxidative and Nitrosative Damage to Iron-Sulfur Centers

Fur-Mediated Activation of Gene Transcription in the Human Pathogen Neisseria gonorrhoeae

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