{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,22]],"date-time":"2026-09-22T08:09:28Z","timestamp":1790064568121,"version":"4.0.1"},"reference-count":20,"publisher":"Wiley","license":[{"start":{"date-parts":[[2026,9,22]],"date-time":"2026-09-22T00:00:00Z","timestamp":1790035200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,9,22]],"date-time":"2026-09-22T00:00:00Z","timestamp":1790035200000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["NSFC 82502762"],"award-info":[{"award-number":["NSFC 82502762"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["mLife"],"abstract":"<jats:title>Impact statement<\/jats:title>\n                  <jats:p>\n                    Fluoroquinolones (FQs) are important for treating fast\u2010growing mycobacterial infections; however, their efficacy can be limited by intrinsic resistance and the emergence of acquired resistance. FQs induce lethal DNA double\u2010strand breaks (DSBs) by targeting topoisomerases. Through a transposon screen in\n                    <jats:italic>Mycobacterium abscessus<\/jats:italic>\n                    , we identified that disruption of\n                    <jats:italic>adnB<\/jats:italic>\n                    , a homologous recombination (HR) gene, markedly sensitized the pathogen to FQs. Subsequent study showed that deleting core HR components (\n                    <jats:italic>adnB<\/jats:italic>\n                    ,\n                    <jats:italic>recO<\/jats:italic>\n                    ,\n                    <jats:italic>recA<\/jats:italic>\n                    ,\n                    <jats:italic>recR<\/jats:italic>\n                    , and\n                    <jats:italic>ruvB<\/jats:italic>\n                    ) increased FQs' susceptibility, while other DSB repair pathways (single\u2010strand annealing or non\u2010homologous end joining) had no effect, demonstrating a unique reliance on HR for FQs' tolerance. Complementation with native or its homolog genes restored the resistance phenotype, indicating a conserved HR\u2010dependent tolerance mechanism in\n                    <jats:italic>M<\/jats:italic>\n                    .\n                    <jats:italic>abscessus<\/jats:italic>\n                    . In a murine model, genetic HR abrogation significantly improved FQs' therapeutic efficacy. These results highlight HR repair as a potential therapeutic target to potentiate FQs' activity and combat drug resistance in\n                    <jats:italic>M<\/jats:italic>\n                    .\n                    <jats:italic>abscessus<\/jats:italic>\n                    infections.\n                  <\/jats:p>","DOI":"10.1002\/mlf2.70103","type":"journal-article","created":{"date-parts":[[2026,9,22]],"date-time":"2026-09-22T07:56:15Z","timestamp":1790063775000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Targeting homologous recombination repair to potentiate fluoroquinolone efficacy in\n                    <i>Mycobacterium abscessus<\/i>"],"prefix":"10.1002","author":[{"given":"Shuai","family":"Wang","sequence":"first","affiliation":[{"name":"State Key Laboratory of Respiratory Disease, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences Guangzhou 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Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences Guangzhou China"},{"name":"University of Chinese Academy of Sciences Beijing China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Buhari","family":"Yusuf","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Respiratory Disease, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences Guangzhou China"},{"name":"China\u2010New Zealand Joint Laboratory on Biomedicine and Health, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences Guangzhou China"},{"name":"Guangdong\u2010Hong Kong\u2010Macao Joint Laboratory of Respiratory Infectious Diseases, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences Guangzhou China"},{"name":"University of Chinese Academy of Sciences Beijing 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