Predicted transmembrane proteins with homology to Mef(A) are not responsible for complementing mef(A) deletion in the

Valeria Fox1, Francesco Santoro1, Gianni Pozzi1

  • 1Department of Medical Biotechnologies, University of Siena, Siena, Italy.

BMC Research Notes
|November 26, 2021
PubMed
Abstract

Insights

The mef(A)-msr(D) gene pair in Streptococcus confers macrolide resistance. Researchers investigated candidate genes in Streptococcus pneumoniae for mef(A) complementation but found no contribution to macrolide efflux.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Genetics

Background:

  • Macrolide resistance in streptococci is mediated by the mef(A)-msr(D) efflux system, an ATP-Binding cassette (ABC) transporter.
  • The mef(A)-msr(D) gene pair, carried by phage ϕ1207.3, can transfer macrolide efflux to Streptococcus pneumoniae.
  • Deletion of mef(A) did not impact erythromycin efflux in pneumococcal strains.

Purpose of the Study:

  • To identify candidate genes responsible for mef(A) complementation in Streptococcus pneumoniae.
  • To investigate the role of putative genes in conferring macrolide resistance.

Main Methods:

  • In silico analysis using the Mef(A) amino acid sequence to identify candidate genes in the S. pneumoniae R6 genome.
  • Construction of isogenic deletion mutants for candidate genes (spr0971, spr1023, spr1932).
  • Erythromycin sensitivity assays and construction of double/triple mutants to assess gene function and synergistic activity.

Main Results:

  • Three candidate genes (spr0971, spr1023, spr1932) were identified through in silico analysis.
  • Deletion mutants of individual candidate genes did not restore erythromycin efflux, indicating they do not complement mef(A) deletion.
  • Double and triple mutants also failed to complement the mef(A) function, suggesting no synergistic activity among these candidates.

Conclusions:

  • The investigated candidate genes (spr0971, spr1023, spr1932) are not involved in mef(A)-mediated macrolide efflux in Streptococcus pneumoniae.
  • Further research is needed to identify the actual genes responsible for mef(A) complementation or alternative mechanisms of macrolide resistance.

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