Identification of SoxS-Regulated Genes in
            <i>Salmonella enterica</i>
            Serovar Typhimurium

Pomposiello, Pablo J.; Demple, Bruce

doi:10.1128/jb.182.1.23-29.2000

Cited by 109 publications

(84 citation statements)

References 35 publications

(28 reference statements)

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“…OmpF expression was decreased in 104-cip, consistent with the role of marRAB and soxRS in the control of its expression (37,40). This mutant also displayed alterations in the LPS ladder.…”

Section: Discussionmentioning

confidence: 54%

Multiple Regulatory Pathways Associated with High-Level Ciprofloxacin and Multidrug Resistance in Salmonella enterica Serovar Enteritidis: Involvement of ramA and Other Global Regulators

O'Regan

Quinn

Pagès

et al. 2009

Antimicrob Agents Chemother

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Mechanisms of antibiotic resistance were examined in nalidixic acid-resistant Salmonella enterica serovar Enteritidis field isolates displaying decreased susceptibility to ciprofloxacin and in in vitro-derived ciprofloxacin-resistant mutants (104-cip and 5408-cip). All field isolates harbored a single gyrA mutation (D87Y). Deletion of acrB and complementation with wild-type gyrA increased quinolone susceptibility. Selection for ciprofloxacin resistance was associated with the development of an additional gyrA (S83F) mutation in 104-cip, novel gyrB (E466D) and parE (V461G) mutations in 5408-cip, overexpression of acrB and decreased susceptibility to nonquinolone antibiotics in both mutants, and decreased OmpF production and altered lipopolysaccharide in 104-cip. Complementation of mutated gyrA and gyrB with wild-type alleles restored susceptibility to quinolones in 104-cip and significantly decreased the ciprofloxacin MIC in 5408-cip. Complementation of parE had no effect on quinolone MICs. Deletion of acrB restored susceptibility to ciprofloxacin and other antibiotics tested. Both soxS and marA were overexpressed in 104-cip, and ramA was overexpressed in 5408-cip. Inactivation of each of these global regulators lowered ciprofloxacin MICs, decreased expression of acrB, and restored susceptibility to other antibiotics. Mutations were found in soxR (R20H) and in soxS (E52K) in 104-cip and in ramR (G25A) in 5408-cip. In conclusion, both efflux activity and a single gyrA mutation contribute to nalidixic acid resistance and reduced ciprofloxacin sensitivity. Ciprofloxacin resistance and decreased susceptibility to multiple antibiotics can result from different genetic events leading to development of target gene mutations, increased efflux activity resulting from differential expression of global regulators associated with mutations in their regulatory genes, and possible altered membrane permeability.

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“…OmpF expression was decreased in 104-cip, consistent with the role of marRAB and soxRS in the control of its expression (37,40). This mutant also displayed alterations in the LPS ladder.…”

Section: Discussionmentioning

confidence: 54%

Multiple Regulatory Pathways Associated with High-Level Ciprofloxacin and Multidrug Resistance in Salmonella enterica Serovar Enteritidis: Involvement of ramA and Other Global Regulators

O'Regan

Quinn

Pagès

et al. 2009

Antimicrob Agents Chemother

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show abstract

“…As in E. coli, increased expression of marA and soxS results in the Mar phenotype [11,31,59]. Recently, Koutsolioutsou et al [31] reported a soxRS-constitutive mutation in a clinical strain of S. enterica serovar Typhimurium that arose with the development of resistance to quinolones during treatment.…”

Section: Active Effluxmentioning

confidence: 99%

“…The marRAB and soxRS operons also occur in Salmonella [11,31,33,58,59,67]. As in E. coli, increased expression of marA and soxS results in the Mar phenotype [11,31,59].…”

Section: Active Effluxmentioning

confidence: 99%

Mechanisms of quinolone resistance in Salmonella

Cloeckaert

Chaslus-Dancla

2001

Vet. Res.

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-As in other Gram-negative bacteria, mechanisms of resistance to quinolones in Salmonella include target gene mutations, active efflux, and decreased outer membrane permeability. However, the exact contribution of these individual mechanisms to resistance, which may nevertheless interplay to reach high-level resistance, has not yet clearly been defined as in other bacteria such as Escherichia coli. This paper reviews the current state of knowledge of quinolone resistance mechanisms in Salmonella by comparison with that of E. coli and future directions of research with particular attention to the recent development of efflux pump inhibitors as possible means of avoiding the emergence and spread of fluoroquinolone resistance.Salmonella / quinolone / resistance / mechanism Résumé -Mécanismes de résistance aux quinolones chez Salmonella. Comme chez les autres bactéries Gram-négatives les mécanismes de résistance aux quinolones chez Salmonella comprennent les mutations dans les gènes cibles, l'efflux actif, et une diminution de la perméabilité de la membrane externe. Cependant la contribution exacte de ces mécanismes individuels, qui peuvent néanmoins interagir pour atteindre des niveaux de résistance élevés, n'a pas encore été clairement définie comme chez d'autres bactéries telle que Escherichia coli. Cette revue présente l'état actuel des connaissances des mécanismes de résistance chez Salmonella par comparaison avec E. coli et des perspectives futures de recherche avec une attention particulière au développement récent d'inhibiteurs de pompes d'efflux comme moyen possible pour éviter l'émergence et la diffusion de la résistance aux fluoroquinolones.Salmonella / quinolone / résistance / mécanisme Vet. Res. 32 (2001) 291-300 291

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“…Ten candidates were identified from ∼10,000 mutants screened. Insertion locations were determined by amplifying and sequencing adjacent genomic DNA as described previously (48).…”

Section: Methodsmentioning

confidence: 99%

Iron and citrate export by a major facilitator superfamily pump regulates metabolism and stress resistance inSalmonellaTyphimurium

Frawley¹,

Crouch²,

Bingham-Ramos³

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

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The efficacy of antibiotics and host defenses has been linked to the metabolic and redox states of bacteria. In this study we report that a stress-induced export pump belonging to the major facilitator superfamily effluxes citrate and iron from the enteric pathogen Salmonella Typhimurium to arrest growth and ameliorate the effects of antibiotics, hydrogen peroxide, and nitric oxide. The transporter, formerly known as MdtD, is now designated IceT (iron citrate efflux transporter). Iron efflux via an iron-chelating tricarboxylic acid cycle intermediate provides a direct link between aerobic metabolism and bacterial stress responses, representing a unique mechanism of resistance to host defenses and antimicrobial agents of diverse classes.

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Identification of SoxS-Regulated Genes in Salmonella enterica Serovar Typhimurium

Cited by 109 publications

References 35 publications

Multiple Regulatory Pathways Associated with High-Level Ciprofloxacin and Multidrug Resistance in Salmonella enterica Serovar Enteritidis: Involvement of ramA and Other Global Regulators

Multiple Regulatory Pathways Associated with High-Level Ciprofloxacin and Multidrug Resistance in Salmonella enterica Serovar Enteritidis: Involvement of ramA and Other Global Regulators

Mechanisms of quinolone resistance in Salmonella

Iron and citrate export by a major facilitator superfamily pump regulates metabolism and stress resistance inSalmonellaTyphimurium

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