Tetracycline Resistance Unassociated with a Change of Cell Wall Permeability in E. Coli

Navashin, S M; Beliavskaya, I. V.; Sazykin, Yu. O.; Gryaznova, N. S.

doi:10.1007/978-3-642-66062-7_27

Cited by 4 publications

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“…Although Tcr cells (defined for this paper as cells bearing the Tcr determinant of TnJO) and Tcs cells (bearing no Tcr determinant) differ 100-to 200-fold in tetracycline susceptibility, cell-free protein synthesis in extracts from Tcr cells was reported to be only severalfold more resistant to tetracycline than that in similar extracts from Tcs cells (14,20). It was possible that a larger difference in Tcr may have existed but had been obscured by some inadequacy of the cell-free assay system.…”

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confidence: 98%

“…CCCP (11). In pH 6.1 buffer with glucose, protein synthesis in the uncB Tcr strain DO-23 (pRT11) was 50% inhibited at about 20 ,ug of tetracycline per ml (this was a lower resistance than that encoded by R222 in the same host, presumably related to a multicopy effect of pRT11 or a transcriptional step-down mutation that may have occurred during cloning [19] (14,20) had been only severalfold. Even this small difference was not reproduced in the present experiments performed on partially intact (toluene-treated) cells.…”

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Effects of toluene permeabilization and cell deenergization on tetracycline resistance in Escherichia coli

McMurry¹,

Hendricks²,

Levy³

1986

Antimicrob Agents Chemother

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Resistance to tetracycline (Tcr) mediated by TnlO and related Tcr determinants involves an inner membrane protein, TET (similar but not identical for different determinants), and a proton motive force-dependent efflux of tetracycline which keeps the drug away from its intracellular target, the ribosome (L. M. McMurry, R. E. Petrucci, Jr., and S. B. Levy, Proc. Natl. Acad. Sci. USA 77:3974-3977, 1980). However, the amount of tetracycline accumulated by bacteria does not always correlate with their resistance levels, suggesting that an additional resistance mechanism may be present. When we permeabilized susceptible and resistant TnlObearing cells with toluene, we found that protein synthesis in the two strains became equally sensitive to tetracycline. Therefore, the protein synthesis machinery was not a source of resistance, and an intact membrane was required for resistance. To determine whether resistance was entirely dependent on energy, we measured susceptibility to tetracycline after inhibition of proton motive force by starvation and specific inhibitors. An 80 to 90% loss of Tcr (measured by protein synthesis) resulted from partial deenergization of resistant cells. A remaining resistance (10-to 20-fold greater than that of susceptible cells) could not be eliminated by further deenergization. These findings indicated that, to a major extent, expression of TnlO resistance required energy, presumably for tetracycline efflux. They also suggested the existence of a small component of Tcr having little or no energy dependence. Whether this component depends on tetracycline efflux or some other mechanism is not known, but presumably both high-and low-energy components of resistance reflect activity of TET protein.

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confidence: 98%

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confidence: 99%