Antibiotic persistence is a phenomenon observed when a subpopulation of genetically susceptible cells survives a prolonged exposure to an otherwise bactericidal concentration of an antibiotic. These ‘persister cells’ or ‘persisters’ survive because their metabolic state renders the antibiotic temporarily ineffective, and later regrow into a susceptible population. Frequency of persisters varies depending on environmental factors and the antibiotic’s mechanism of action, however it is increased in ‘highly-persistent’ genetic mutants.
Antibiotic persistence is widely recognized as a public health concern as it prolongs treatment time and contributes to recurring infections. Recently, it has also been demonstrated that persistence can be a ‘stepping-stone’ to genetic resistance, further highlighting a need for the development of anti-persister agents (1).
Persister cells are notoriously difficult to investigate as they are a small subpopulation with unique physiology. In this study we employed flow cytometry and fluorescence-activated cell sorting, combined with the use of fluorescent intracellular pH (2) and NADH/NAD+ (3) biosensors to characterise the persister phenotype on a single-cell level prior to, during and post antibiotic exposure in the model organism Escherichia coli. Persisters have been previously shown to have a lower intracellular pH (4) and redox activity (5) than antibiotic-sensitive cells, however the mechanisms behind this remain unclear. We focus on two highly-persistent E. coli strains, HipQ which contains a non-synonymous mutation in putative electron transfer protein ydiR and ΔydcI lacking pH stress response regulator ydcI (6). We aim to develop a universal framework for using biosensors to investigate persister physiology and to gain further understanding of how intracellular pH and redox activity affects antibiotic persistence.