ArticleAntimicrobial agents and chemotherapy2012
Molecular basis for different levels of tet(M) expression in Streptococcus pneumoniae clinical isolates.
Article in Antimicrobial agents and chemotherapy, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- Integrative genomic characterization of five Pediococcus acidilactici strains reveals differing probiotic safety profiles.PloS one · 2025Article
- Extensive/Multidrug-Resistant Pneumococci Detected in Clinical Respiratory Tract Samples in Southern Sweden Are Closely Related to International Multidrug-Resistant Lineages.Frontiers in cellular and infection microbiology · 2022Article
- Transferable Multidrug-Resistance Plasmid Carrying a Novel Macrolide-Clindamycin Resistance Gene,Antimicrobial agents and chemotherapy · 2020Article
- Multiple mutations and increased RNA expression in tetracycline-resistant Streptococcus pneumoniae as determined by genome-wide DNA and mRNA sequencing.The Journal of antimicrobial chemotherapy · 2015Article
- Molecular characterization of Streptococcus agalactiae isolates harboring small erm(T)-carrying plasmids.Antimicrobial agents and chemotherapy · 2014Article
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Authors and funding
8 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Seventy-four unrelated clinical isolates of Streptococcus pneumoniae harboring the tet(M) gene were studied. Seven strains with low tetracycline (Tc) MICs (0.25 to 0.5 μg/ml) were found to harbor truncated tet(M) alleles that were inactivated by different frameshift mutations. In contrast, five strains bore deletions in the tet(M) promoter region, among which four displayed increased Tc MICs (16 to 64 μg/ml). The same promoter mutations were detected in Tc-resistant mutants selected in vitro from various susceptible strains. Sequence analysis revealed that these deletions might impede the formation of the transcriptional attenuator located immediately upstream of tet(M). Expression in Enterococcus faecalis of a tet(M) reporter gene transcribed from these promoter mutants conferred a level of Tc resistance similar to that observed in the parental S. pneumoniae strains. These results show that different levels of Tc susceptibility found in clinical isolates of S. pneumoniae can be explained by frameshift mutations within tet(M) and by alterations of the upstream transcriptional attenuator.
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