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
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Research Support, Non-U.S. Gov't
MeSH terms
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Aminoglycosides / pharmacology
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Anti-Bacterial Agents / pharmacology*
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Bacterial Proteins / metabolism
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Enzyme Inhibitors / pharmacology
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Fluoroquinolones / pharmacology
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Gene Expression Regulation, Bacterial
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Mitomycin / pharmacology*
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Protein Synthesis Inhibitors / pharmacology
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Rec A Recombinases / biosynthesis
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Rec A Recombinases / genetics
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Recombinant Fusion Proteins / metabolism
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Regulon / drug effects
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SOS Response, Genetics
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Streptococcus pneumoniae / drug effects*
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Streptococcus pneumoniae / genetics*
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Streptococcus pneumoniae / metabolism
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Transformation, Bacterial*
Substances
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Aminoglycosides
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Anti-Bacterial Agents
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Bacterial Proteins
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Enzyme Inhibitors
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Fluoroquinolones
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Protein Synthesis Inhibitors
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Recombinant Fusion Proteins
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competence factor, Streptococcus
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Mitomycin
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Rec A Recombinases