Plasmid-Mediated Tetracycline Resistance in E. coli

Levy, Stuart B.; McMurry, Laura M.; Onigman, Philip; Saunders, Richard M.

doi:10.1007/978-3-7091-8501-8_12

Cited by 33 publications

(40 citation statements)

References 31 publications

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“…All those determinants examined so far specify an inducible -43-kDa inner membrane Tet protein whose amino acid sequences are similar, but not identical (43). Later work by several groups showed that the inner membrane Tet protein is the likely transport protein (15,33,43,47).…”

Section: Identifying Active Effluxmentioning

confidence: 99%

Active efflux mechanisms for antimicrobial resistance

Levy

1992

Antimicrob Agents Chemother

444

310

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Section: Identifying Active Effluxmentioning

confidence: 99%

Active efflux mechanisms for antimicrobial resistance

Levy

1992

Antimicrob Agents Chemother

444

310

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“…Tetracycline uptake studie8. Uptake of tetracycline was assessed by uptake of [7-3H]tetracycline, which was received as a powder (0.6 to 1.0 Ci/mmol) from New England Nuclear Corp. Fresh solutions of the radioactive drug in methanol were prepared each week, since breakdown products accumulate in solution and preferentially bind to cell walls (26,27 (35). The initial internal tetracycline concentration was assumed to be zero, and the permeability coefficient was then the velocity divided by the external tetracycline concentration in micromoles per cm3 (20,29).…”

Section: Materials and Metlodsmentioning

confidence: 99%

“…not correlate with levels of sensitivity (32). We have been particularly interested in this property because we are concemed with the mechanism of resistance to tetracycline, particularly that mediated by plasmids (24,25,27). For this reason we have investigated in more detail the mechanism by which tetracycline is accumulated in sensitive cells.…”

mentioning

confidence: 99%

Two Transport Systems for Tetracycline in Sensitive Escherichia coli : Critical Role for an Initial Rapid Uptake System Insensitive to Energy Inhibitors

McMurry¹,

Levy

1978

Antimicrob Agents Chemother

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Escherichia coli sensitivity to tetracycline involves transport and accumulation of the antibiotic within the cell by two different uptake systems: an initial rapid uptake, which occun over the initial 6 min of contact of the cell with tetracycline, and a slower uptake system, which continues indefinitely and whose rate of uptake is 1/10 that of the rapid system. Only the slow uptake system is blocked by inhibitors of energy-driven systems; it appears to be particularly dependent upon energy from oxidative phosphorylation. Althoughboth uptake systems lead to accumulation ofintracellular tetracycline and contribute to the cell's sensitivity, the rapid uptake system appears to be the more important. While these studies confirm active transport of tetracycline into the cell, they demonstrate that a critical uptake system which appears insensitive to metabolic inhibitors occurs initially.The tetracyclines are effective bacteriostatic antimicrobial agents. They were introduced in the beginning of the 1950s and received widespread acceptance because of their broad-spectrum activity against gram-negative as well as gram-positive bacterial infections (17). The drugs inhibit protein synthesis by interfering with the binding of aminoacyl tRNA to the ribosome-mRNA complex (36). The site of action of the drug appears to be codon-anticodon recognition (19).Studies of tetracycline metabolism have demonstrated active uptake ofthe drug into sensitive cells (1, 15). However, the amounts of drug taken up by different strains of Escherichia coli did. not correlate with levels of sensitivity (32). We have been particularly interested in this property because we are concemed with the mechanism of resistance to tetracycline, particularly that mediated by plasmids (24,25,27). For this reason we have investigated in more detail the mechanism by which tetracycline is accumulated in sensitive cells. From these studies we have determined that the sensitive cell has two uptake systems for tetracycline, only one of which appears sensitive to metabolic inhibitors. An initial uptake occurs, which appears to reach an equilibrium with the tetracycline in the medium after 6 min. A slow, second uptake system then is evident, which accumulates tetracycline over a period of hours. It is the slow uptake system that is sensitive to energy inhibitors.Experiments with mutants uncoupled in oxidative phosphorylation confimned the presence of two uptake systems and indicated that sensitivity to the drug can be conferred by the rapid uptake system alone.MATERIALS AND METLODS

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“…Mechanism 1 (conferring tetracycline resistance) might therefore result from protection of membranebound ribosomes and mechanism 3 (conferring joint minocycline and tetracycline resistance) from protection of cytoplasmic ribosomes. In this context, Levy and co-workers (Levy et al, 1977;Levy & McMurry, 1978) have already suggested that TnlO-mediated resistance results partially from protection of ribosomes.…”

Section: Discussionmentioning

confidence: 99%

Evidence for More Than One Mechanism of Plasmid-determined Tetracycline Resistance in Escherichia coli

1980

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The basis of tetracycline resistance mediated by TetA determinants and joint resistance to tetracycline and minocycline coded by TetB determinants was investigated. The TetA class of determinants was represented by those carried on plasmids pSC101, RPl and pIP7 and TetB by TnlO. The relationships between expression of tetracycline and minocycline resistance and accumulation of these antibiotics suggest that there are three mechanisms of plasmid-determined resistance conferring (1) about a 10-to 20-fold increase in resistance to tetracycline that is not associated with decreased antibiotic accumulation, (2) a 4-to ?' -fold increase in resistance to tetracycline that is associated with decreased drug accumulation, and (3) about a 2-to 3-fold increase in resistance to both tetracycline and minocycline that is not associated with decreased accumulation of either antibiotic. Mechanism 1 was coded by the tetracycline resistance determinant of pSClOl (TetA), mechanisms 1 and 2 by the determinants in RP1 and pIP7 (TetA) and all three mechanisms by TnlO (TetB).

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Plasmid-Mediated Tetracycline Resistance in E. coli

Cited by 33 publications

References 31 publications

Active efflux mechanisms for antimicrobial resistance

Active efflux mechanisms for antimicrobial resistance

Two Transport Systems for Tetracycline in Sensitive Escherichia coli : Critical Role for an Initial Rapid Uptake System Insensitive to Energy Inhibitors

Evidence for More Than One Mechanism of Plasmid-determined Tetracycline Resistance in Escherichia coli

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