Timing of DNA damage responses impacts persistence to fluoroquinolones
Abstract
Bacterial persisters are able to survive high concentrations of antibiotics that kill their genetically identical kin. Their tolerances are thought to arise from decreased activity of cellular processes, which limits damage from antibiotics. However, persistence to fluoroquinolones in growth-inhibited populations is not as cut-and-dried, with survivors of treatment exhibiting similar DNA damage as cells that die. In this article, we use a model system of persistence to reveal that the timing of events, such as DNA repair, following fluoroquinolone treatment is critical to survival and show that the same is true for WT populations. These data highlight the importance of processes following antibiotic treatments to persister phenotypes and establish that timing matters for genetically susceptible bacteria struggling to survive fluoroquinolone treatments.
Document Details
- Document Type
- Pub Defense Publication
- Publication Date
- Jun 18, 2018
- Source ID
- 10.1073/pnas.1804218115
Entities
People
- Mark P. Brynildsen
- Wendy W. K. Mok
Organizations
- Army Research Office
- Charles H. Revson Foundation
- Princeton University