Antibiotic stress induces genetic transformability in the human pathogen Streptococcus pneumoniae

Science. 2006 Jul 7;313(5783):89-92. doi: 10.1126/science.1127912.

Abstract

Natural transformation is a widespread mechanism for genetic exchange in bacteria. Aminoglycoside and fluoroquinolone antibiotics, as well as mitomycin C, a DNA-damaging agent, induced transformation in Streptococcus pneumoniae. This induction required an intact competence regulatory cascade. Furthermore, mitomycin C induction of recA was strictly dependent on the development of competence. In response to antibiotic stress, S. pneumoniae, which lacks an SOS-like system, exhibited genetic transformation. The design of antibiotherapy should take into consideration this potential of a major human pathogen to increase its rate of genetic exchange in response to antibiotics.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aminoglycosides / pharmacology
  • Anti-Bacterial Agents / pharmacology*
  • Bacterial Proteins / metabolism
  • Enzyme Inhibitors / pharmacology
  • Fluoroquinolones / pharmacology
  • Gene Expression Regulation, Bacterial
  • Mitomycin / pharmacology*
  • Protein Synthesis Inhibitors / pharmacology
  • Rec A Recombinases / biosynthesis
  • Rec A Recombinases / genetics
  • Recombinant Fusion Proteins / metabolism
  • Regulon / drug effects
  • SOS Response, Genetics
  • Streptococcus pneumoniae / drug effects*
  • Streptococcus pneumoniae / genetics*
  • Streptococcus pneumoniae / metabolism
  • Transformation, Bacterial*

Substances

  • Aminoglycosides
  • Anti-Bacterial Agents
  • Bacterial Proteins
  • Enzyme Inhibitors
  • Fluoroquinolones
  • Protein Synthesis Inhibitors
  • Recombinant Fusion Proteins
  • competence factor, Streptococcus
  • Mitomycin
  • Rec A Recombinases