Abstract
ABSTRACTBacterial 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.
Highlights
Bacterial persistence is a transient, nonheritable physiological state that provides tolerance to bactericidal antibiotics
Formation, and the SOS response [3, 5,6,7]. cyclic AMP (cAMP)-CRP has previously been implicated in the negative regulation of persistence in uropathogenic Escherichia coli (UPEC), wherein transposon insertions that disrupted cyaA and the promoter for crp resulted in increased survival upon exposure to the -lactam antibiotic ampicillin [8]
To further characterize the role that cAMP has in the generation of persister cells, we first compared the killing dynamics of the ΔcyaA mutant with those of the wild type (WT) in cultures exposed to ampicillin
Summary
Bacterial persistence is a transient, nonheritable physiological state that provides tolerance to bactericidal antibiotics. Increased survival was observed in ΔcyaA mutant cultures exposed to the cell wall-acting antibiotics meropenem, cefoxitin, and oxacillin (Fig. 1a). To further characterize the role that cAMP has in the generation of persister cells, we first compared the killing dynamics of the ΔcyaA mutant with those of the wild type (WT) in cultures exposed to ampicillin.
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