Transcriptional Regulation of<i>sitABCD</i>of<i>Salmonella enterica</i>Serovar Typhimurium by MntR and Fur

Ikeda, Jack S.; Janakiraman, Anuradha; Kehres, David G.; Maguire, Michael E.; Slauch, James M.

doi:10.1128/jb.187.3.912-922.2005

Cited by 87 publications

(123 citation statements)

References 40 publications

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“…As previously demonstrated (22,26,28,38), we observed that mntH is repressed by manganese and induced by EDTA (Fig. 2).…”

Section: Resultssupporting

confidence: 87%

“…Upon binding to manganese, MntR binds promoter DNA to repress or activate transcription of its target genes (15,30). In enterobacteria, the only genes known to be regulated by MntR when this work began were mntH and sitABCD, encoding manganese transporters, of which laboratory strains of Escherichia coli only possess mntH (22,26,38). In some Gram-positive bacteria, the MntR analog seems to regulate a large set of genes and mediate a more global response (36).…”

mentioning

confidence: 99%

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The Escherichia coli MntR Miniregulon Includes Genes Encoding a Small Protein and an Efflux Pump Required for Manganese Homeostasis

2011

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Manganese is a critical micronutrient for cells, serving as an enzyme cofactor and protecting against oxidative stress. Yet, manganese is toxic in excess and little is known about its distribution in cells. Bacteria control intracellular manganese levels by the transcription regulator MntR. When this work began, the only Escherichia coli K-12 gene known to respond to manganese via MntR repression was mntH, which encodes a manganese importer. We show that mntS (formerly the small RNA gene rybA) is repressed by manganese through MntR and encodes an unannotated 42-amino-acid protein. Overproduction of MntS causes manganese sensitivity, while a lack of MntS perturbs proper manganese-dependent repression of mntH. We also provide evidence that mntP (formerly yebN), which encodes a putative efflux pump, is positively regulated by MntR. Deletion of mntP leads to profound manganese sensitivity and to elevated intracellular manganese levels. This work thus defines two new proteins involved in manganese homeostasis and suggests mechanisms for their action.

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“…As previously demonstrated (22,26,28,38), we observed that mntH is repressed by manganese and induced by EDTA (Fig. 2).…”

Section: Resultssupporting

confidence: 87%

mentioning

confidence: 99%

The Escherichia coli MntR Miniregulon Includes Genes Encoding a Small Protein and an Efflux Pump Required for Manganese Homeostasis

2011

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“…6B) suggests that Fe also plays a role in the Mn homeostasis. Similar Mn-mediated activation of Fur-and Fe-mediated activation of MntR was also observed earlier (10,35,36). Our data also suggest that the MntRFe 2ϩ complex is able to suppress mntH expression (see Fig.…”

Section: A Robust Link Between Hflx and Mn Homeostasis Is Discoveredsupporting

confidence: 73%

“…However, alternative mechanisms of regulation, viz. Mn-mediated activation of Fur, Fe-mediated activation of MntR, or Mnmediated inactivation of Zur, have also been proposed (10,30,34,35,36). In our present study, accumulation of Mn in the Mnperturbed ⌬hflX strain increases Zn and decreases Fe levels, suggesting that an influx of Mn is capable of affecting both Fe and Zn regulatory networks (Fig.…”

Section: Fig 3 Hflx-mediated Mn Homeostasis Is Not Linked To the Mntrsupporting

confidence: 53%

Novel MntR-Independent Mechanism of Manganese Homeostasis in Escherichia coli by the Ribosome-Associated Protein HflX

et al. 2014

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Manganese is a micronutrient required for activities of several important enzymes under conditions of oxidative stress and iron starvation. In Escherichia coli, the manganese homeostasis network primarily constitutes a manganese importer (MntH) and an exporter (MntP), which are regulated by the MntR dual regulator. In this study, we find that deletion of E. coli hflX, which encodes a ribosome-associated GTPase with unknown function, renders extreme manganese sensitivity characterized by arrested cell growth, filamentation, lower rate of replication, and DNA damage. We demonstrate that perturbation by manganese induces unprecedented influx of manganese in ⌬hflX cells compared to that in the wild-type E. coli strain. Interestingly, our study indicates that the imbalance in manganese homeostasis in the ⌬hflX strain is independent of the MntR regulon. Moreover, the influx of manganese leads to a simultaneous influx of zinc and inhibition of iron import in ⌬hflX cells. In order to review a possible link of HflX with the phage life cycle, we performed a lysis-lysogeny assay to show that the Mn-perturbed ⌬hflX strain reduces the frequency of lysogenization of the phage. This observation raises the possibility that the induced zinc influx in the manganese-perturbed ⌬hflX strain stimulates the activity of the zinc-metalloprotease HflB, the key determinant of the lysis-lysogeny switch. Finally, we propose that manganese-mediated autophosphorylation of HflX plays a central role in manganese, zinc, and iron homeostasis in E. coli cells.

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“…In view of this, we must consider that other Fur-regulated genes, namely those with complex regulation involving additional factors, may not have been identified in these studies. Reports for other organisms have described a number of regulatory circuits that respond to changes in iron levels, including the stringent control pathways (72) and those involving Crp (83) or the manganese regulator MntR (38,40). These networks could potentially influence the iron-dependent Fur regulon in V. cholerae.…”

Section: Discussionmentioning

confidence: 99%

Iron and Fur Regulation in Vibrio cholerae and the Role of Fur in Virulence

et al. 2005

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Regulation of iron uptake and utilization is critical for bacterial growth and for prevention of iron toxicity. In many bacterial species, this regulation depends on the iron-responsive master regulator Fur. In this study we report the effects of iron and Fur on gene expression in Vibrio cholerae. We show that Fur has both positive and negative regulatory functions, and we demonstrate Fur-independent regulation of gene expression by iron. Nearly all of the known iron acquisition genes were repressed by Fur under iron-replete conditions. In addition, genes for two newly identified iron transport systems, Feo and Fbp, were found to be negatively regulated by iron and Fur. Other genes identified in this study as being induced in low iron and in the fur mutant include those encoding superoxide dismutase (sodA), fumarate dehydratase (fumC), bacterioferritin (bfr), bacterioferritin-associated ferredoxin (bfd), and multiple genes of unknown function. Several genes encoding ironcontaining proteins were repressed in low iron and in the fur mutant, possibly reflecting the need to reserve available iron for the most critical functions. Also repressed in the fur mutant, but independently of iron, were genes located in the V. cholerae pathogenicity island, encoding the toxin-coregulated pilus (TCP), and genes within the V. cholerae mega-integron. The fur mutant exhibited very weak autoagglutination, indicating a possible defect in expression or assembly of the TCP, a major virulence factor of V. cholerae. Consistent with this observation, the fur mutant competed poorly with its wild-type parental strain for colonization of the infant mouse gut.

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Transcriptional Regulation ofsitABCDofSalmonella entericaSerovar Typhimurium by MntR and Fur

Cited by 87 publications

References 40 publications

The Escherichia coli MntR Miniregulon Includes Genes Encoding a Small Protein and an Efflux Pump Required for Manganese Homeostasis

The Escherichia coli MntR Miniregulon Includes Genes Encoding a Small Protein and an Efflux Pump Required for Manganese Homeostasis

Novel MntR-Independent Mechanism of Manganese Homeostasis in Escherichia coli by the Ribosome-Associated Protein HflX

Iron and Fur Regulation in Vibrio cholerae and the Role of Fur in Virulence

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