Journal
DNA REPAIR
Volume 71, Issue -, Pages 108-117Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.dnarep.2018.08.014
Keywords
Base excision repair; Cell death; Antibiotics; Reactive oxygen species; Thymineless death; 8-oxo-dG
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Funding
- NIH [R01CA021615, R35ES028303]
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Numerous lethal stresses in bacteria including antibiotics, thymineless death, and MalE-LacZ expression trigger an increase in the production of reactive oxygen species. This results in the oxidation of the nucleotide pool by radicals produced by Fenton chemistry. Following the incorporation of these oxidized nucleotides into the genome, the cell's unsuccessful attempt to repair these lesions through base excision repair (BER) contributes causally to the lethality of these stresses. We review the evidence for this phenomenon of incomplete BER-mediated cell death and discuss how better understanding this pathway could contribute to the development of new antibiotics.
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