{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,21]],"date-time":"2026-09-21T18:13:11Z","timestamp":1790014391307,"version":"4.0.1"},"reference-count":77,"publisher":"Public Library of Science (PLoS)","issue":"9","license":[{"start":{"date-parts":[[2026,9,21]],"date-time":"2026-09-21T00:00:00Z","timestamp":1789948800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100000060","name":"National Institute of Allergy and Infectious Diseases","doi-asserted-by":"publisher","award":["R21AI182745"],"award-info":[{"award-number":["R21AI182745"]}],"id":[{"id":"10.13039\/100000060","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000057","name":"National Institute of General Medical Sciences","doi-asserted-by":"publisher","award":["T32GM007388"],"award-info":[{"award-number":["T32GM007388"]}],"id":[{"id":"10.13039\/100000057","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["www.plosgenetics.org"],"crossmark-restriction":false},"short-container-title":["PLoS Genet"],"abstract":"<jats:p>\n                    Stationary-phase cultures contain high abundances of persisters, which are bacterial cells that are hyper-tolerant to antibiotics due to phenotypic reasons. Fluoroquinolones (FQs) are one of the most effective antibiotic classes for the treatment of non-growing bacteria, such as those found in stationary-phase cultures, and persisters in those populations have been found to survive FQ treatment by repairing the DNA damage caused by the antibiotic rather than by avoiding damage through inactivity. Interestingly, previous work demonstrated that transient growth inhibition after the conclusion of FQ treatment significantly increased persister levels from stationary-phase\n                    <jats:italic>Escherichia coli<\/jats:italic>\n                    populations if\n                    <jats:italic>recA<\/jats:italic>\n                    , a mediator of homologous recombination (HR), or\n                    <jats:italic>uvrD<\/jats:italic>\n                    , a component of nucleotide excision repair (NER), were present. Here, we sought to identify additional epistatic interaction partners in that persister recovery network by deleting DNA repair enzymes known to interact with RecA or UvrD. We found that\n                    <jats:italic>uvrA<\/jats:italic>\n                    ,\n                    <jats:italic>uvrB<\/jats:italic>\n                    , and\n                    <jats:italic>mfd<\/jats:italic>\n                    also epistatically interact with\n                    <jats:italic>recA<\/jats:italic>\n                    in FQ persister recovery, whereas\n                    <jats:italic>recB<\/jats:italic>\n                    and\n                    <jats:italic>recC<\/jats:italic>\n                    are additional epistatic interaction partners of\n                    <jats:italic>uvrD<\/jats:italic>\n                    . While these results indicated that HR and NER can contribute to persister recovery, different combinations of genetic mutants suggested that the phenomenon is more nuanced than compensation for loss of one repair pathway by another. Specifically, loss of\n                    <jats:italic>recA<\/jats:italic>\n                    had farther reaching epistatic consequences than loss of other HR genes, and loss of\n                    <jats:italic>uvrD<\/jats:italic>\n                    had a greater impact on the network than any other NER gene. Delving deeper into the roles of RecA and UvrD, we found that the recombination function of RecA, via RecA(N304D), and helicase function of UvrD, via UvrD(R284A), were required for their participation in FQ persister recovery. Collectively, the data presented here deepen understanding of the roles of HR and NER machinery in the recovery FQ persisters and further emphasize the important roles of RecA and UvrD in this phenomenon.\n                  <\/jats:p>","DOI":"10.1371\/journal.pgen.1012305","type":"journal-article","created":{"date-parts":[[2026,9,21]],"date-time":"2026-09-21T17:52:31Z","timestamp":1790013151000},"page":"e1012305","update-policy":"https:\/\/doi.org\/10.1371\/journal.pgen.corrections_policy","source":"Crossref","is-referenced-by-count":0,"title":["Genetic analysis of epistasis between nucleotide excision repair and homologous recombination in the recovery of persisters after fluoroquinolone treatment"],"prefix":"10.1371","volume":"22","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-5400-1207","authenticated-orcid":true,"given":"Nashaly","family":"Soto-Echevarria","sequence":"first","affiliation":[{"name":"Princeton University","place":["Princeton, New Jersey, United States of America"],"department":["Department of Molecular Biology"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Annabel S.","family":"Lemma","sequence":"additional","affiliation":[{"name":"Princeton University","place":["Princeton, New Jersey, United States of America"],"department":["Department of Chemical and Biological Engineering"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5707-8894","authenticated-orcid":true,"given":"Mark P.","family":"Brynildsen","sequence":"additional","affiliation":[{"name":"Princeton University","place":["Princeton, New Jersey, United States of America"],"department":["Department of Molecular Biology"]},{"name":"Princeton University","place":["Princeton, New Jersey, United States of America"],"department":["Department of Chemical and Biological Engineering"]},{"name":"Omenn-Darling Bioengineering Institute, Princeton University","place":["Princeton, New Jersey, United States of America"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"340","published-online":{"date-parts":[[2026,9,21]]},"reference":[{"issue":"5690","key":"pgen.1012305.ref001","doi-asserted-by":"crossref","first-page":"1622","DOI":"10.1126\/science.1099390","article-title":"Bacterial persistence as a phenotypic switch","volume":"305","author":"NQ Balaban","year":"2004","journal-title":"Science"},{"issue":"7","key":"pgen.1012305.ref002","doi-asserted-by":"crossref","first-page":"441","DOI":"10.1038\/s41579-019-0196-3","article-title":"Definitions and guidelines for research on antibiotic persistence","volume":"17","author":"NQ Balaban","year":"2019","journal-title":"Nat Rev Microbiol"},{"issue":"3","key":"pgen.1012305.ref003","doi-asserted-by":"crossref","first-page":"219","DOI":"10.1093\/femsre\/fux001","article-title":"Formation, physiology, ecology, evolution and clinical importance of bacterial persisters","volume":"41","author":"B Van den 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