Anaerobic Regulation of
            <i>Shigella flexneri</i>
            Virulence: ArcA Regulates
            <i>fur</i>
            and Iron Acquisition Genes

Boulette, Megan L.; Payne, Shelley M.

doi:10.1128/jb.00621-07

Cited by 55 publications

(69 citation statements)

References 67 publications

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“…The cytoplasm is a reducing environment (44) which likely keeps a portion of the small pool of accessible iron in the ferrous form, even in the presence of oxygen. This is consistent with our earlier observation that the Sit system provided iron to intracellular bacteria when the cultured cells were growing aerobically but not in an anaerobic environment (3).…”

Section: Discussionsupporting

confidence: 82%

“…Surprisingly, the S. flexneri sit genes were repressed when the cells were grown anaerobically (3), although the homologous sitABCD genes in Salmonella encode a ferrous iron uptake system (20,63). Consistent with aerobic induction, the Sit system was sufficient to support plaque formation by S. flexneri under aerobic, but not anaerobic, conditions (3).…”

mentioning

confidence: 58%

“…As previously noted in E. coli K-12 (19), expression of the feo ferrous iron transport operon was induced under anaerobic conditions, where ferrous iron should predominate over ferric iron. In contrast, the aerobactin genes were induced aerobically, consistent with their role in ferric iron uptake (3). Surprisingly, the S. flexneri sit genes were repressed when the cells were grown anaerobically (3), although the homologous sitABCD genes in Salmonella encode a ferrous iron uptake system (20,63).…”

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confidence: 92%

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Genetics and Virulence Association of the Shigella flexneri Sit Iron Transport System

et al. 2009

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The sit-encoded iron transport system is present within pathogenicity islands in all Shigella spp. and some pathogenic Escherichia coli strains. The islands contain numerous insertion elements and sequences with homology to bacteriophage genes. The Shigella flexneri sit genes can be lost as a result of deletion within the island. The formation of deletions was dependent upon RecA and occurred at relatively high frequency. This suggests that the sit region is inherently unstable, yet sit genes are maintained in all of the clinical isolates tested. Characterization of the sitABCD genes in S. flexneri indicates that they encode a ferrous iron transport system, although the genes are induced aerobically. The sit genes provide a competitive advantage to S. flexneri growing within epithelial cells, and a sitA mutant is outcompeted by the wild type in cultured epithelial cells. The Sit system is also required for virulence in a mouse lung model. The sitA mutant was able to infect the mice and induce a protective immune response but was avirulent compared to its wild-type parent strain.

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Section: Discussionsupporting

confidence: 82%

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confidence: 58%

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confidence: 92%

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Genetics and Virulence Association of the Shigella flexneri Sit Iron Transport System

et al. 2009

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“…6B). Of note, FNR has been shown to positively regulate transcription of metal transporters, such as nikABCDE nickel transport genes and feoABC iron uptake genes of E. coli (34,73) and feoABC, sitABCD, and fhuA iron uptake genes of Shigella flexneri (10,74). To our knowledge, FNR-mediated regulation of genes involved in zinc acquisition or homeostasis has not previously been demonstrated.…”

Section: Discussionmentioning

confidence: 90%

A Novel Zinc Binding System, ZevAB, Is Critical for Survival of Nontypeable Haemophilus influenzae in a Murine Lung Infection Model

et al. 2011

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Nontypeable Haemophilus influenzae (NTHI) is a Gram-negative bacterial pathogen that causes upper and lower respiratory infections. Factors required for pulmonary infection by NTHI are not well understood. Previously, using high-throughput insertion tracking by deep sequencing (HITS), putative lung colonization factors were identified. Also, previous research indicates that secreted disulfide-dependent factors are important for virulence of H. influenzae. In the present study, HITS data were compared with an informatics-based list of putative substrates of the periplasmic oxidoreductase DsbA to find and characterize secreted virulence factors. This analysis resulted in identification of the "zinc binding essential for virulence" (zev) locus consisting of zevA (HI1249) and zevB (HI1248). NTHI mutants of zevA and zevB grew normally in rich medium but were defective for colonization in a mouse lung model. Mutants also exhibited severe growth defects in medium containing EDTA and were rescued by supplementation with zinc. Additionally, purified recombinant ZevA was found to bind to zinc with high affinity. Together, these data demonstrate that zevAB is a novel virulence factor important for zinc utilization of H. influenzae under conditions where zinc is limiting. Furthermore, evidence presented here suggests that zinc limitation is likely an important mechanism for host defense against pathogens during lung infection.

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“…It is conceivable that the vci genes respond to a signal that is present in the human host but not in the mouse. One reason to expect that a system such as the Vci system, which increases iron uptake via a ferrous iron transporter, is important for in vivo iron acquisition is that the lumen of the human intestine is likely anaerobic or microaerophilic, conditions known to promote the ferrous form of iron and the expression of ferrous iron transport systems such as Feo (7,24) while repressing ferric iron uptake systems (7). In several pathogens of the digestive tract, ferrous iron uptake via Feo is critical for establishing gastric (64) or intestinal infection in the host (40,59,62).…”

Section: Discussionmentioning

confidence: 99%

Vibrio choleraeVciB Promotes Iron Uptake via Ferrous Iron Transporters

et al. 2008

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Vibrio cholerae uses a variety of strategies for obtaining iron in its diverse environments. In this study we report the identification of a novel iron utilization protein in V. cholerae, VciB. The vciB gene and its linked gene, vciA, were isolated in a screen for V. cholerae genes that permitted growth of an Escherichia coli siderophore mutant in low-iron medium. The vciAB operon encodes a predicted TonB-dependent outer membrane receptor, VciA, and a putative inner membrane protein, VciB. VciB, but not VciA, was required for growth stimulation of E. coli and Shigella flexneri strains in low-iron medium. Consistent with these findings, TonB was not needed for VciB-mediated growth. No growth enhancement was seen when vciB was expressed in an E. coli or S. flexneri strain defective for the ferrous iron transporter Feo. Supplying the E. coli feo mutant with a plasmid encoding either E. coli or V. cholerae Feo, or the S. flexneri ferrous iron transport system Sit, restored VciB-mediated growth; however, no stimulation was seen when either of the ferric uptake systems V. cholerae Fbp and Haemophilus influenzae Hit was expressed. These data indicate that VciB functions by promoting iron uptake via a ferrous, but not ferric, iron transport system. VciB-dependent iron accumulation via Feo was demonstrated directly in iron transport assays using radiolabeled iron. A V. cholerae vciB mutant did not exhibit any growth defects in either in vitro or in vivo assays, possibly due to the presence of other systems with overlapping functions in this pathogen.

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Anaerobic Regulation of Shigella flexneri Virulence: ArcA Regulates fur and Iron Acquisition Genes

Cited by 55 publications

References 67 publications

Genetics and Virulence Association of the Shigella flexneri Sit Iron Transport System

Genetics and Virulence Association of the Shigella flexneri Sit Iron Transport System

A Novel Zinc Binding System, ZevAB, Is Critical for Survival of Nontypeable Haemophilus influenzae in a Murine Lung Infection Model

Vibrio choleraeVciB Promotes Iron Uptake via Ferrous Iron Transporters

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