Mutations in respiratory complex I promote antibiotic persistence through alterations in intracellular acidity and protein synthesis

Abstract

Antibiotic persisters are phenotypic variants within an isogenic bacterial population that are transiently tolerant to antibiotic treatment. Here, the authors provide evidence that cytoplasmic acidification, amplified by a compromised respiratory complex I, can act as a signaling hub for perturbed metabolic homeostasis in antibiotic persisters.