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.

ABSTRACT:

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 genom

SUBMITTER: Fox V 

PROVIDER: S-EPMC8620141 | biostudies-literature | 2021 Nov

REPOSITORIES: biostudies-literature