Incomplete base excision repair contributes to cell death from antibiotics and other stresses
Name
nihms-1015060.pdf
Description
Accepted version
Size
583.68 KB
Format
Adobe PDF
Checksum (MD5)
546a444adca411347075b4d7102c91e7
Author(s)
Gruber, Charley C.
Walker, Graham C.
Date Issued
November 2018
Journal
DNA Repair
Publisher
Elsevier BV
Citation
Gruber, Charley C. and Graham C. Walker. “Incomplete base excision repair contributes to cell death from antibiotics and other stresses.” DNA Repair 71 (2018): 108-117 © 2018 The Author(s)
Version
Author's final manuscript
Abstract
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.
MIT Department
Massachusetts Institute of Technology. Department of Biology
Terms of Use
Creative Commons Attribution-NonCommercial-NoDerivs License
Persistent DSpace Link
DOI of Published Version
https://doi.org/10.1016/j.dnarep.2018.08.014
