SOS response induction by β-lactams and bacterial defense against antibiotic lethality
SOS response induction by β-lactams and bacterial defense against antibiotic lethality
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DOI：
10.1126/science.1101630
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发表时间：
2004-09-10
期刊：
影响因子：
56.9
通讯作者：
Cohen, SN
中科院分区：
文献类型：
--
作者：
Miller, C;Thomsen, LE;Cohen, SN
SOS反应通过在DNA损伤修复期间抑制细胞分裂来帮助细菌繁殖。我们报告的ftsl基因产物，青霉素结合蛋白3，无论是β-内酰胺类抗生素或基因突变的失活诱导SOS在大肠杆菌通过DpiBA双组分信号转导系统。该事件需要SOS促进recA和莱克萨基因以及dpiA，短暂停止细菌细胞分裂，使细菌能够存活至其他致命的抗生素暴露。我们的研究结果揭示了有缺陷的细胞等待合成作为细菌SOS反应的意外引发剂，表明β-内酰胺抗生素是这种反应的细胞外刺激物，并证明了减轻抗菌剂致死性的新机制。
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.