Analysis of the genetic requirements for inducible multiple-antibiotic resistance associated with the mar locus in Escherichia coli

Sulavik, Mark C.; Gambino, Laura; Miller, Paul

doi:10.1128/jb.176.24.7754-7756.1994

Cited by 24 publications

(23 citation statements)

References 18 publications

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“…A reduction in SAL-inducible multiple antibiotic resistance was observed (Table 3), as evidenced by increased susceptibility to ampicillin, chloramphenicol, and tetracycline compared to the isogenic marA ϩ parent strain. These results are similar to those reported for E. coli ⌬mar strains (13,53). Hypersensitivity to chloramphenicol and tetracycline in this strain in the absence of SAL was not observed.…”

Section: Fig 1 Locations and Associated Phenotypes Of ␥␦-Transposonsupporting

confidence: 81%

“…The two proteins have identical helix-turnhelix DNA-binding motifs, and it follows that the target promoter sites recognized by these proteins are likely to be conserved between the two organisms. Analogous to what was previously reported for E. coli (13,53), S. typhimurium marA strains are attenuated for SAL-inducible antibiotic resistance in comparison to wild-type strains (Table 3); however, such attenuation is not complete. Thus, SAL induces Par by both mar-dependent and mar-independent pathways, as was previously reported for E. coli (13).…”

Section: Discussionmentioning

confidence: 61%

“…Two examples are SlyA, which is necessary for S. typhimurium infection of BALB/c mice (33), and PecS, and Erwinia chrysanthemi regulatory protein controlling extracellular enzymes involved in soft rot disease of plants (46). Second, in the absence of an inducing agent, marRAB is weakly expressed when E. coli is cultured on standard laboratory media (12,13,25,39,50,53). As the identity of the true inducer of marRAB is not known, it is conceivable that it is present at some stage of infection.…”

mentioning

confidence: 99%

“…A 1.1-kbp marRAB operon regulates multiple antibiotic resistance (12,19,36) by controlling expression of at least 10 unlinked genes (22,44,48,51), two of which, acrA and acrB, are absolutely required for resistance (44). The marRAB operon consists of (i) an operator-promoter region (marO) from which divergent transcripts are generated; (ii) marR, encoding a repressor of the marRAB operon (12,50,53); (iii) marA, encoding a positive transcriptional regulator of unlinked genes whose modulation affects antibiotic resistance (12,15,19,21,22,30); and (iv) marB, a gene of unknown function. Previously characterized mar mutants contain mutations in either marR or marO, which disrupt autorepression and lead to increased expression of marA and, consequently, activation of the regulon (2,12,19,36).…”

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confidence: 99%

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The Salmonella typhimurium mar locus: molecular and genetic analyses and assessment of its role in virulence

Sulavik¹,

Dazer²,

Miller³

1997

J Bacteriol

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The marRAB operon is a regulatory locus that controls multiple drug resistance in Escherichia coli. marA encodes a positive regulator of the antibiotic resistance response, acting by altering the expression of unlinked genes. marR encodes a repressor of marRAB transcription and controls the production of MarA in response to environmental signals. A molecular and genetic study of the homologous operon in Salmonella typhimurium was undertaken, and the role of marA in virulence in a murine model was assessed. Expression of E. coli marA (marA Ec ) present on a multicopy plasmid in S. typhimurium resulted in a multiple antibiotic resistance (Mar) phenotype, suggesting that a similar regulon exists in this organism. A genomic plasmid library containing S. typhimurium chromosomal sequences was introduced into an E. coli strain that was deleted for the mar locus and contained a single-copy marR-lacZ translational fusion. Plasmid clones that contained both S. typhimurium marR (marR St ) and marA (marA St ) genes were identified as those that were capable of repressing expression of the fusion and which resulted in a Mar phenotype. The predicted amino acid sequences of MarR St , MarA St , and MarB St were 91, 86, and 42% identical, respectively, to the same genes from E. coli, while the operator/promoter region of the operon was 86% identical to the same 98-nucleotide-upstream region in E. coli. The marRAB transcriptional start sites for both organisms were determined by primer extension, and a marRAB St transcript of ϳ1.1 kb was identified by Northern blot analysis. Its accumulation was shown to be inducible by sodium salicylate. Open reading frames flanking the marRAB operon were also conserved. An S. typhimurium marA disruption strain was constructed by an allelic exchange method and compared to the wild-type strain for virulence in a murine BALB/c infection model. No effect on virulence was noted. The endogenous S. typhimurium plasmid that is associated with virulence played no role in marA-mediated multiple antibiotic resistance. Taken together, the data show that the S. typhimurium mar locus is structurally and functionally similar to marRAB Ec and that a lesion in marA St has no effect on S. typhimurium virulence for BALB/c mice.

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Section: Fig 1 Locations and Associated Phenotypes Of ␥␦-Transposonsupporting

confidence: 81%

Section: Discussionmentioning

confidence: 61%

mentioning

confidence: 99%

mentioning

confidence: 99%

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The Salmonella typhimurium mar locus: molecular and genetic analyses and assessment of its role in virulence

Sulavik¹,

Dazer²,

Miller³

1997

J Bacteriol

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124

113

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“…The alleles that affect the Mar phenotype are located in the marRAB operon (1,23). The marA gene encodes a positive regulator of antibiotic resistance whose sequence shows strong similarity to those of such transcriptional regulators as SoxS, XylS, and AraC (1,7,8), while marR encodes a repressor of the marRAB operon (1).…”

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confidence: 99%

AcrAB efflux pump plays a major role in the antibiotic resistance phenotype of Escherichia coli multiple-antibiotic-resistance (Mar) mutants

1996

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Multiple-antibiotic-resistance (Mar) mutants of Escherichia coli are resistant to a wide variety of antibiotics, and increased active efflux is known to be responsible for the resistance to some drugs. The identity of the efflux system, however, has remained unknown. By constructing an isogenic set of E. coli K-12 strains, we showed that the marR1 mutation was incapable of increasing the resistance level in the absence of the AcrAB efflux system. This experiment identified the AcrAB system as the major pump responsible for making the Mar mutants resistant to many agents, including tetracycline, chloramphenicol, ampicillin, nalidixic acid, and rifampin.

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Bacterial Membrane, a Key for Controlling Drug Influx and Efflux

et al. 2013

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Analysis of the genetic requirements for inducible multiple-antibiotic resistance associated with the mar locus in Escherichia coli

Cited by 24 publications

References 18 publications

The Salmonella typhimurium mar locus: molecular and genetic analyses and assessment of its role in virulence

The Salmonella typhimurium mar locus: molecular and genetic analyses and assessment of its role in virulence

AcrAB efflux pump plays a major role in the antibiotic resistance phenotype of Escherichia coli multiple-antibiotic-resistance (Mar) mutants

Bacterial Membrane, a Key for Controlling Drug Influx and Efflux

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