J I Ross, E A Eady, J H Cove, W J Cunliffe
Department of Microbiology, University of Leeds, United Kingdom. micjir@leeds.ac.uk
Antimicrobial agents and chemotherapy 1998 JulA genetic basis for tetracycline resistance in cutaneous propionibacteria was suggested by comparing the nucleotide sequences of the 16S rRNA genes from 16 susceptible and 21 resistant clinical isolates and 6 laboratory-selected tetracycline-resistant mutants of a susceptible strain. Fifteen clinical isolates resistant to tetracycline were found to have cytosine instead of guanine at a position cognate with Escherichia coli 16S rRNA base 1058 in a region important for peptide chain termination and translational accuracy known as helix 34. Cytosine at base 1058 was not detected in the laboratory mutants or the tetracycline-susceptible strains. The apparent mutation was recreated by site-directed mutagenesis in the cloned E. coli ribosomal operon, rrnB, encoded by pKK3535.E. coli strains carrying the mutant plasmid were more resistant to tetracycline than those carrying the wild-type plasmid both in MIC determinations and when grown in tetracycline-containing liquid medium. These data are consistent with a role for the single 16S rRNA base mutation in clinical tetracycline resistance in cutaneous propionibacteria.
J I Ross, E A Eady, J H Cove, W J Cunliffe. 16S rRNA mutation associated with tetracycline resistance in a gram-positive bacterium. Antimicrobial agents and chemotherapy. 1998 Jul;42(7):1702-5
PMID: 9661007
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