Oxidation of the Guanine Nucleotide Pool Underlies Cell Death by Bactericidal Antibiotics

被引:384
作者
Foti, James J. [1 ]
Devadoss, Babho [1 ]
Winkler, Jonathan A. [2 ]
Collins, James J. [3 ,4 ,5 ]
Walker, Graham C. [1 ]
机构
[1] MIT, Dept Biol, Cambridge, MA 02139 USA
[2] Boston Univ, Program Mol Biol Cell Biol & Biochem, Boston, MA 02215 USA
[3] Boston Univ, Howard Hughes Med Inst, Dept Biomed Engn, Boston, MA 02215 USA
[4] Boston Univ, Ctr BioDynam, Boston, MA 02215 USA
[5] Harvard Univ, Wyss Inst Biol Inspired Engn, Boston, MA 02118 USA
关键词
DOUBLE-STRAND BREAKS; MUTT-TYPE ENZYME; ESCHERICHIA-COLI; DNA-POLYMERASES; HYDROGEN-PEROXIDE; PROTEIN; REPLICATION; MECHANISMS; DAMAGE; MUTAGENESIS;
D O I
10.1126/science.1219192
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
A detailed understanding of the mechanisms that underlie antibiotic killing is important for the derivation of new classes of antibiotics and clinically useful adjuvants for current antimicrobial therapies. Our efforts to understand why DinB (DNA polymerase IV) overproduction is cytotoxic to Escherichia coli led to the unexpected insight that oxidation of guanine to 8-oxo-guanine in the nucleotide pool underlies much of the cell death caused by both DinB overproduction and bactericidal antibiotics. We propose a model in which the cytotoxicity of beta-lactams and quinolones predominantly results from lethal double-strand DNA breaks caused by incomplete repair of closely spaced 8-oxo-deoxyguanosine lesions, whereas the cytotoxicity of aminoglycosides might additionally result from mistranslation due to the incorporation of 8-oxo-guanine into newly synthesized RNAs.
引用
收藏
页码:315 / 319
页数:5
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