{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,27]],"date-time":"2026-02-27T02:52:55Z","timestamp":1772160775767,"version":"3.50.1"},"reference-count":80,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2019,3,27]],"date-time":"2019-03-27T00:00:00Z","timestamp":1553644800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["31670137 31700128"],"award-info":[{"award-number":["31670137 31700128"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Molecular Microbiology"],"published-print":{"date-parts":[[2019,6]]},"abstract":"<jats:title>Summary<\/jats:title>\n                  <jats:p>\n                    Bacterial antibiotic resistance, a global health threat, is caused by plasmid transfer or genetic mutations. Quinolones are important antibiotics, partially because they are fully synthetic and resistance genes are unlikely to exist in nature; nonetheless, quinolone resistance proteins have been identified. The mechanism by which plasmid\u2010borne quinolone resistance proteins promotes the selection of quinolone\u2010resistant mutants is unclear. Here, we show that QnrB increases the bacterial mutation rate. Transcriptomic and genome sequencing analyses showed that QnrB promoted gene abundance near the origin of replication (\n                    <jats:italic>oriC<\/jats:italic>\n                    ). In addition, the QnrB expression level correlated with the replication origin to terminus (\n                    <jats:italic>oriC<\/jats:italic>\n                    \/\n                    <jats:italic>ter<\/jats:italic>\n                    ) ratio, indicating QnrB\u2010induced DNA replication stress. Our results also show that QnrB is a DnaA\u2010binding protein that may act as an activator of DNA replication initiation. Interaction of QnrB with DnaA promoted the formation of the DnaA\u2010\n                    <jats:italic>oriC<\/jats:italic>\n                    open complex, which leads to DNA replication over\u2010initiation. Our data indicate that plasmid\u2010borne QnrB increases bacterial mutation rates and that genetic changes can alleviate the fitness cost imposed by transmitted plasmids. Derivative mutations may impair antibiotic efficacy and threaten the value of antibiotic treatments. Enhanced understanding of how bacteria adapt to the antibiotic environment will lead to new therapeutic strategies for antibiotic\u2010resistant infections.\n                  <\/jats:p>","DOI":"10.1111\/mmi.14235","type":"journal-article","created":{"date-parts":[[2019,3,6]],"date-time":"2019-03-06T02:40:22Z","timestamp":1551840022000},"page":"1529-1543","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":16,"title":["The plasmid\u2010borne quinolone resistance protein QnrB, a novel DnaA\u2010binding protein, increases the bacterial mutation rate by triggering DNA replication stress"],"prefix":"10.1111","volume":"111","author":[{"given":"Xiaojing","family":"Li","sequence":"first","affiliation":[{"name":"CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of Microbiology Chinese Academy of Sciences Beijing 100101 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