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Objectives  In 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.    Results  In 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.    Supplementary Information  The online version contains supplementary material available at 10.1186/s13104-021-05856-6.

bmc research notes

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