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Genetic complexity of fusidic acid-resistant small colony variants (SCV) in Staphylococcus aureus

Jonas Lannergård1, Sha Cao, Tobias Norström

  • 1Uppsala University, Department of Cell and Molecular Biology, The Biomedical Center, Uppsala, Sweden.

Plos One
|December 6, 2011
PubMed

Insights

FusE mutants of Staphylococcus aureus exhibit resistance to fusidic acid and form small colony variants (SCVs). These mutants possess mutations in rplF, with some also showing auxotrophy due to mutations in hemin or menadione biosynthesis genes.

Area of Science:

  • Microbiology
  • Bacterial Genetics
  • Molecular Biology

Background:

  • FusE mutants are characterized as fusidic acid-resistant small colony variants (SCVs) in Staphylococcus aureus.
  • These SCVs can be isolated using aminoglycosides and all possess mutations in the rplF gene, which encodes ribosomal protein L6.

Purpose of the Study:

  • To investigate the genetic basis of auxotrophy observed in FusE SCVs.
  • To determine if additional mutations beyond rplF contribute to the FusE SCV phenotype.

Main Methods:

  • Genetic sub-grouping of FusE SCVs.
  • Genome sequencing of FusE mutants.
  • Reversion analysis to confirm gene function.

Main Results:

  • FusE SCVs were classified into three distinct genetic sub-groups.
  • Some FusE SCVs harbor additional mutations in genes essential for hemin biosynthesis (hem genes).
  • Other FusE SCVs carry mutations in genes critical for menadione biosynthesis (men genes).

Conclusions:

  • The combination of mutations in rplF and genes involved in hemin or menadione biosynthesis explains the SCV and auxotrophic characteristics of FusE mutants.
  • This study elucidates the complex genetic architecture underlying specific phenotypes in Staphylococcus aureus SCVs.

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