Journal
SCIENCE
Volume 305, Issue 5690, Pages 1629-1631Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1101630
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Funding
- NIAID NIH HHS [R01 AI08619] Funding Source: Medline
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The SOS response aids bacterial propagation by inhibiting cell division during repair of DNA damage. We report that inactivation of the ftsl gene product, penicillin binding protein 3, by either beta-lactam antibiotics or genetic mutation induces SOS in Escherichia coli through the DpiBA two-component signal transduction system. This event, which requires the SOS-promoting recA and lexA genes as well as dpiA, transiently halts bacterial cell division, enabling survival to otherwise lethal antibiotic exposure. Our findings reveal defective cell wait synthesis as an unexpected initiator of the bacterial SOS response, indicate that beta-lactam antibiotics are extracellular stimuli of this response, and demonstrate a novel mechanism for mitigation of antimicrobial lethality.
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