SUMMARYThe resistance levels conferred by the T-determinants in four R-factors to Tetracycline and Minocycline in cells ofEscherichia coliK 12, before and after induction of maximum resistance by treatment with sub-inhibitory concentrations of the drugs, are measured by simple growth-and-challenge tests. The effect of a plasmid TKwhich confers tetracycline resistance on its hostKlebsiella aerogenesis tested in the same way. The five T-determinants fall into a high-level and a low-level group for resistance, the former giving 3- to 4-fold higher resistance in both induced and uninduced cells than the latter. The T-determinants all confer much lower resistance to Minocycline (a tetracycline molecule modified at the C-6 and C-7 positions) than to Tetracycline. The main cause of this difference is that cells carrying a T-determinant exclude Minocycline much less efficiently than Tetracycline, but in addition Minocycline is less effective than Tetracycline in inducing increased resistance. These results are discussed in the light of a model put forward to explain the inducible nature of R-factor resistance to the tetracyclines.

SUMMARYEleven mutants of R-factor R57 have been isolated which show constitutive expression of resistance to tetracycline (Tc). These derepressed (Tdr) mutants all gave a much greater resistance to Tc and to its analogue, minocycline, than could be obtained by optimal induction of cells carrying the wild-type (T+) determinant. Cells carrying each of the Tdr mutants together with T+of either R6-S or of a plasmid found inEscherichia colimi19 showed inducible Tc resistance, indicating that the Tdr mutants were all recessive, i.e. of repressor-negative type. Tdr1 was not recessive to the T-determinant of RP1, suggesting that the repressor gene products of the T-determinants in R57 and RP1 have different specificities.

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