Incomplete base excision repair contributes to cell death from antibiotics and other stresses
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 thes...
| Main Authors: | , |
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| Other Authors: | |
| Format: | Article |
| Language: | English |
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Elsevier BV
2020
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| Online Access: | https://hdl.handle.net/1721.1/124921 |
| _version_ | 1826206544300081152 |
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| author | Gruber, Charley C. Walker, Graham C. |
| author2 | Massachusetts Institute of Technology. Department of Biology |
| author_facet | Massachusetts Institute of Technology. Department of Biology Gruber, Charley C. Walker, Graham C. |
| author_sort | Gruber, Charley C. |
| collection | MIT |
| description | 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. |
| first_indexed | 2024-09-23T13:34:37Z |
| format | Article |
| id | mit-1721.1/124921 |
| institution | Massachusetts Institute of Technology |
| language | English |
| last_indexed | 2024-09-23T13:34:37Z |
| publishDate | 2020 |
| publisher | Elsevier BV |
| record_format | dspace |
| spelling | mit-1721.1/1249212022-10-01T15:48:11Z Incomplete base excision repair contributes to cell death from antibiotics and other stresses Gruber, Charley C. Walker, Graham C. Massachusetts Institute of Technology. Department of Biology 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. National Institutes of Health (U.S.) (Grant R01CA021615) National Institutes of Health (U.S.) (Grant R35ES028303) 2020-04-29T14:15:11Z 2020-04-29T14:15:11Z 2018-11 2020-01-30T19:10:57Z Article http://purl.org/eprint/type/JournalArticle 1568-7864 https://hdl.handle.net/1721.1/124921 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) en 10.1016/j.dnarep.2018.08.014 DNA Repair Creative Commons Attribution-NonCommercial-NoDerivs License http://creativecommons.org/licenses/by-nc-nd/4.0/ application/pdf Elsevier BV PMC |
| spellingShingle | Gruber, Charley C. Walker, Graham C. Incomplete base excision repair contributes to cell death from antibiotics and other stresses |
| title | Incomplete base excision repair contributes to cell death from antibiotics and other stresses |
| title_full | Incomplete base excision repair contributes to cell death from antibiotics and other stresses |
| title_fullStr | Incomplete base excision repair contributes to cell death from antibiotics and other stresses |
| title_full_unstemmed | Incomplete base excision repair contributes to cell death from antibiotics and other stresses |
| title_short | Incomplete base excision repair contributes to cell death from antibiotics and other stresses |
| title_sort | incomplete base excision repair contributes to cell death from antibiotics and other stresses |
| url | https://hdl.handle.net/1721.1/124921 |
| work_keys_str_mv | AT grubercharleyc incompletebaseexcisionrepaircontributestocelldeathfromantibioticsandotherstresses AT walkergrahamc incompletebaseexcisionrepaircontributestocelldeathfromantibioticsandotherstresses |