Format

Send to

Choose Destination
See comment in PubMed Commons below
Antimicrob Agents Chemother. 2012 Oct;56(10):5040-5. doi: 10.1128/AAC.00939-12. Epub 2012 Jul 16.

Molecular basis for different levels of tet(M) expression in Streptococcus pneumoniae clinical isolates.

Author information

1
Service de Microbiologie AP-HP, Hôpital Européen Georges Pompidou, Paris, France.

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.

PMID:
22802249
PMCID:
PMC3457367
DOI:
10.1128/AAC.00939-12
[Indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for HighWire Icon for PubMed Central
    Loading ...
    Support Center