{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Leon G"],"funding":["National Institute of Allergy and Infectious Diseases","Princeton University School of Engineering and Applied Science","NIAID NIH HHS","Omenn Darling Bioengineering Institute"],"pagination":["e1011840"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12413089"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["21(9)"],"pubmed_abstract":["Studies have shown that DNA damage repair systems, including homologous recombination (HR) and the SOS response, are important for fluoroquinolone (FQ) persistence of Escherichia coli, which has been the workhorse organism of persister research. We sought to explore whether those systems are also important for FQ persistence of Pseudomonas aeruginosa, a common cause of lung infections in cystic fibrosis patients, which can be treated with FQs such as ciprofloxacin (CIP). Notably, P. aeruginosa has important differences in its DNA damage repair capabilities compared to E. coli that include the machinery needed to conduct non-homologous end-joining (NHEJ), Ku and LigD. Using a genetic approach, we found that loss of HR significantly depressed persister levels of P. aeruginosa to CIP during s"],"journal":["PLoS genetics"],"pubmed_title":["Conservation and divergence of ciprofloxacin persister survival mechanisms between Pseudomonas aeruginosa and Escherichia coli."],"pmcid":["PMC12413089"],"funding_grant_id":["R21AI182745","R21 AI185486","R21AI185486","R21 AI182745"],"pubmed_authors":["Brynildsen MP","Leon G"],"additional_accession":[]},"is_claimable":false,"name":"Conservation and divergence of ciprofloxacin persister survival mechanisms between Pseudomonas aeruginosa and Escherichia coli.","description":"Studies have shown that DNA damage repair systems, including homologous recombination (HR) and the SOS response, are important for fluoroquinolone (FQ) persistence of Escherichia coli, which has been the workhorse organism of persister research. We sought to explore whether those systems are also important for FQ persistence of Pseudomonas aeruginosa, a common cause of lung infections in cystic fibrosis patients, which can be treated with FQs such as ciprofloxacin (CIP). Notably, P. aeruginosa has important differences in its DNA damage repair capabilities compared to E. coli that include the machinery needed to conduct non-homologous end-joining (NHEJ), Ku and LigD. Using a genetic approach, we found that loss of HR significantly depressed persister levels of P. aeruginosa to CIP during s","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Sep","modification":"2026-06-01T23:25:00.344Z","creation":"2026-05-23T03:07:41.994Z"},"accession":"S-EPMC12413089","cross_references":{"pubmed":["40892829"],"doi":["10.1371/journal.pgen.1011840"]}}