Cyclic AMP Regulates Bacterial Persistence through Repression of the Oxidative Stress Response and SOS-Dependent DNA Repair in Uropathogenic Escherichia coli

• Main Authors: Roberto C. Molina-Quiroz, Cecilia Silva-Valenzuela, Jennifer Brewster, Eduardo Castro-Nallar, Stuart B. Levy, Andrew Camilli, Michael S. Gilmore
• Format: Article
• Language: English
• Published: American Society for Microbiology 2018-01-01
• Series: mBio
• Online Access: http://mbio.asm.org/cgi/content/full/9/1/e02144-17

Bacterial persistence is a transient, nonheritable physiological state that provides tolerance to bactericidal antibiotics. The stringent response, toxin-antitoxin modules, and stochastic processes, among other mechanisms, play roles in this phenomenon. How persistence is regulated is relatively ill defined. Here we show that cyclic AMP, a global regulator of carbon catabolism and other core processes, is a negative regulator of bacterial persistence in uropathogenic Escherichia coli, as measured by survival after exposure to a β-lactam antibiotic. This phenotype is regulated by a set of genes leading to an oxidative stress response and SOS-dependent DNA repair. Thus, persister cells tolerant to cell wall-acting antibiotics must cope with oxidative stress and DNA damage and these processes are regulated by cyclic AMP in uropathogenic E. coli.