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Naturally occurring Staphylococcus epidermidis plasmid expressing constitutive macrolide-lincosamide-streptogramin B

Insights

This study reveals the molecular basis for constitutive macrolide-lincosamide-streptogramin B (MLS) resistance in Staphylococcus epidermidis. A specific deletion in the ermM gene explains its continuous expression, unlike inducible resistance.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Genetics

Background:

  • Macrolide-lincosamide-streptogramin B (MLS) resistance is a significant challenge in bacterial infections.
  • Constitutive expression of resistance genes, unlike inducible expression, leads to continuous antibiotic resistance.
  • The plasmid pNE131 from Staphylococcus epidermidis carries a gene mediating constitutive MLS resistance.

Purpose of the Study:

  • To investigate the molecular mechanisms underlying the constitutive expression of MLS resistance.
  • To characterize the ermM gene responsible for constitutive MLS resistance in pNE131.
  • To compare the ermM gene with the inducible ermC gene.

Main Methods:

  • Restriction and functional mapping of the pNE131 plasmid.
  • Nucleotide sequencing of the ermM gene.
  • Sequence comparison between ermM and ermC genes.

Main Results:

  • The ermM gene, responsible for constitutive MLS resistance, was sequenced.
  • ermM shares 98% sequence homology with ermC, the inducible MLS resistance determinant.
  • A 107-base-pair deletion in the 5' promoter region of ermM, compared to ermC, was identified as the cause of constitutive expression.

Conclusions:

  • Constitutive MLS resistance mediated by ermM is due to a specific deletion in its promoter region.
  • This deletion in ermM removes sequences critical for attenuation, leading to continuous methylase expression and resistance.
  • Understanding these mechanisms is crucial for combating antibiotic resistance.

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