{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Van den Bergh B"],"funding":["Dutch Research Council (NWO)"],"pagination":["546"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8795404"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["13(1)"],"pubmed_abstract":["Antibiotic persistence describes the presence of phenotypic variants within an isogenic bacterial population that are transiently tolerant to antibiotic treatment. Perturbations of metabolic homeostasis can promote antibiotic persistence, but the precise mechanisms are not well understood. Here, we use laboratory evolution, population-wide sequencing and biochemical characterizations to identify mutations in respiratory complex I and discover how they promote persistence in Escherichia coli. We show that persistence-inducing perturbations of metabolic homeostasis are associated with cytoplasmic acidification. Such cytoplasmic acidification is further strengthened by compromised proton pumping in the complex I mutants. While RpoS regulon activation induces persistence in the wild type, the "],"journal":["Nature communications"],"pubmed_title":["Mutations in respiratory complex I promote antibiotic persistence through alterations in intracellular acidity and protein synthesis."],"pmcid":["PMC8795404"],"funding_grant_id":["864.11.001"],"pubmed_authors":["Radzikowski JL","Schmidt A","Kimkes TEP","Van den Bergh B","Dewachter L","Schimpf J","Burschel S","Loncar N","Schramke H","Meijer T","Heinemann M","Vedelaar SR","Fauvart M","Michiels J","Michiels JE","Friedrich T"],"additional_accession":[]},"is_claimable":false,"name":"Mutations in respiratory complex I promote antibiotic persistence through alterations in intracellular acidity and protein synthesis.","description":"Antibiotic persistence describes the presence of phenotypic variants within an isogenic bacterial population that are transiently tolerant to antibiotic treatment. Perturbations of metabolic homeostasis can promote antibiotic persistence, but the precise mechanisms are not well understood. Here, we use laboratory evolution, population-wide sequencing and biochemical characterizations to identify mutations in respiratory complex I and discover how they promote persistence in Escherichia coli. We show that persistence-inducing perturbations of metabolic homeostasis are associated with cytoplasmic acidification. Such cytoplasmic acidification is further strengthened by compromised proton pumping in the complex I mutants. While RpoS regulon activation induces persistence in the wild type, the ","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Jan","modification":"2026-05-30T22:59:23.938Z","creation":"2024-11-13T22:40:33.148Z"},"accession":"S-EPMC8795404","cross_references":{"pubmed":["35087069"],"doi":["10.1038/s41467-022-28141-x"]}}