ArticleBMC research notes2021
Predicted transmembrane proteins with homology to Mef(A) are not responsible for complementing mef(A) deletion in the mef(A)-msr(D) macrolide efflux system in Streptococcus pneumoniae.
Article in BMC research notes, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 10 citations in OpenAlex.
- The novel pseudo-compound transposon TnMicrobial genomics · 2026Article
- Unveiling the Resistome Landscape in Peri-Implant Health and Disease.Journal of clinical medicine · 2025Article
- Effects of Antimicrobial Agents Used for Dental Treatments: Impacts on the Human Oral Ecosystem and the Resistome.Advances in experimental medicine and biology · 2025Review
- A nisin-inducible chromosomal gene expression system based on ICE Tn5253 of Streptococcus pneumoniae, transferable among streptococci and enterococci.World journal of microbiology & biotechnology · 2024Article
- Chlorhexidine digluconate mouthwash alters the oral microbial composition and affects the prevalence of antimicrobial resistance genes.Frontiers in microbiology · 2024Article
- TheJournal of bacteriology · 2023Article
- Antibiotic Resistance ofAntibiotics (Basel, Switzerland) · 2023Article
- Streptococcus pyogenes Φ1207.3 Is a Temperate Bacteriophage Carrying the Macrolide Resistance Gene PairMicrobiology spectrum · 2023Article
- Successful Intra- but Not Inter-species Recombination ofFrontiers in microbiology · 2022Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
objectivesIn streptococci, the type M resistance to macrolides is due to the mef(A)-msr(D) efflux transport system of the ATP-Binding cassette (ABC) superfamily, where it is proposed that mef(A) codes for the transmembrane channel and msr(D) for the two ATP-binding domains. Phage ϕ1207.3 of Streptococcus pyogenes, carrying the mef(A)-msr(D) gene pair, is able to transfer the macrolide efflux phenotype to Streptococcus pneumoniae. Deletion of mef(A) in pneumococcal ϕ1207.3-carrying strains did not affect erythromycin efflux. In order to identify candidate genes likely involved in complementation of mef(A) deletion, the Mef(A) amino acid sequence was used as probe for database searching.
resultsIn silico analysis identified 3 putative candidates in the S. pneumoniae R6 genome, namely spr0971, spr1023 and spr1932. Isogenic deletion mutants of each candidate gene were constructed and used in erythromycin sensitivity assays to investigate their contribution to mef(A) complementation. Since no change in erythromycin sensitivity was observed compared to the parental strain, we produced double and triple mutants to assess the potential synergic activity of the selected genes. Also these mutants did not complement the mef(A) function.
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