Department of Biology, Massachusetts Institute of Technology, Cambridge, MA, 02139, United States.
Department of Biology, Massachusetts Institute of Technology, Cambridge, MA, 02139, United States.
DNA Repair (Amst). 2018 Nov;71:108-117. doi: 10.1016/j.dnarep.2018.08.014. Epub 2018 Aug 25.
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.
许多细菌的致死应激，包括抗生素、胸腺嘧啶缺乏死亡和 MalE-LacZ 表达，都会引发活性氧物质的产生增加。这导致 Fenton 化学产生的自由基氧化核苷酸池。在这些氧化核苷酸被掺入基因组后，细胞通过碱基切除修复（BER）来修复这些损伤的尝试失败，这是这些应激导致细胞死亡的原因。我们回顾了这一不完全的 BER 介导的细胞死亡现象的证据，并讨论了更好地理解这一途径如何有助于开发新的抗生素。
