16S rRNA Mutation Associated with Tetracycline Resistance in a Gram-Positive Bacterium
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A 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.
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Mutation of G1058 to cytosine causes resistance to tetracycline.
“Mutation of G1058 to cytosine causes resistance to Tc (Ross et al. 1998”
From The Structural Basis for the Action of the Antibiotics Tetracycline, Pactamycin, and Hygromycin B on the 30S Ribosomal Subunit (2000) · cites this paper as Ross et al. 1998
Tetracyclines bind primarily to the 30S ribosomal subunit.
“Tcs bind primarily to the 30S ribosomal subunit (Ross et al. 1998”
From The Structural Basis for the Action of the Antibiotics Tetracycline, Pactamycin, and Hygromycin B on the 30S Ribosomal Subunit (2000) · cites this paper as Ross et al. 1998
16S rRNA mutations seen in H. pylori and P. acnes that confer resistance to tetracycline are in close proximity to the primary binding site.
“(v) 16S rRNA mutations seen in H. pylori (19, 55) and P. acnes (40) that confer resistance to tetracycline are in close proximity to the primary binding site.”
From Ribosomal Protection Proteins and Their Mechanism ofTetracyclineResistance (2003) · cites this paper as [40]
Mutations within helices h31 and h34 of 16S rRNA confer tetracycline resistance in H. pylori and P. acnes.
“mutations within helices h31 and h34 of 16S rRNA have been reported to confer tetracycline resistance in Helicobacter pylori and Propionibacterium acnes (31, 40).”
From Target- and resistance-based mechanistic studies with TP-434, a novel fluorocycline antibiotic (2012) · cites this paper as [31]
The residue identified in tetracycline-resistant P. acnes mutants is directly adjacent to the primary binding site, but this mutation did not mediate tetracycline resistance in H. pylori.
“The residue identified in the tetracycline-resistant P. acnes mutants is directly adjacent to the primary binding site (4, 23, 25), but this mutation did not mediate tetracycline resistance in H. pylori.”
From Mutations in the 16S rRNA Genes of<i>Helicobacter pylori</i>Mediate Resistance to Tetracycline (2002) · cites this paper as [25]
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References 27 · Cited by 194
- Authors
- Ross, J. I., Eady, E. A., Cove, J. H., & Cunliffe, W. J.
- Affiliations
- University of Leeds (GB)
- Leeds General Infirmary (GB)
- ORCID
- Eady, E. Anne
- Venue
- Antimicrobial Agents and Chemotherapy
- Publisher
- American Society for Microbiology
- Published
- 1998-07
- Volume
- 42
- Issue
- 7
- Pages
- 1702-1705
- ISSN
- 0066-4804 (ISSN-L)
- 1098-6596
- PMC
- PMC105669
- OpenAlex
- W1725324815
- Cited by
- 194
- References
- 27
- Citations by year
- 2026: 4 · 2025: 5 · 2024: 3 · 2023: 5 · 2022: 6 · 2021: 10 · 2020: 6 · 2019: 4 · 2018: 8 · 2017: 8 · 2016: 4 · 2015: 7 · 2014: 16 · 2013: 9 · 2012: 10
- FWCI
- 2.76
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Antimicrobial Agents and Chemotherapy (publishedVersion)
- PubMed Central (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Infectious Diseases › Antimicrobial Resistance in Staphylococcus
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Medicine › Antibiotic Resistance in Bacteria
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › RNA and protein synthesis mechanisms
- Keywords
- tetracycline resistance, 16S rRNA mutations, site-directed mutagenesis, clinical isolates, minimum inhibitory concentration
- MeSH terms
- DNA, Bacterial, Escherichia coli, Gram-Positive Bacteria, Microbial Sensitivity Tests, Plasmids, Propionibacterium, RNA, Ribosomal, 16S, Tetracycline Resistance, Mutagenesis, Site-Directed
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