{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,1]],"date-time":"2026-09-01T03:27:42Z","timestamp":1788233262894,"version":"build-2803163510"},"reference-count":0,"publisher":"SAGE Publications","issue":"2","license":[{"start":{"date-parts":[[2003,6,1]],"date-time":"2003-06-01T00:00:00Z","timestamp":1054425600000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Microbial Drug Resistance"],"published-print":{"date-parts":[[2003,6]]},"abstract":"<jats:p>\n                    Measuring antibiotic-induced killing relies on time-consuming biological tests. The firefly luciferase gene (\n                    <jats:italic toggle=\"yes\">luc<\/jats:italic>\n                    ) was successfully used as a reporter gene to assess antibiotic efficacy rapidly in\n         slow-growing\n                    <jats:italic toggle=\"yes\">Mycobacterium tuberculosis<\/jats:italic>\n                    . We tested whether\n                    <jats:italic toggle=\"yes\">luc<\/jats:italic>\n                    expression could also provide a rapid evaluation of bactericidal drugs in\n                    <jats:italic toggle=\"yes\">Streptococcus gordonii<\/jats:italic>\n                    . The suicide vectors\n         pFW5luc and a modified version of pJDC9 carrying a promoterless\n                    <jats:italic toggle=\"yes\">luc<\/jats:italic>\n                    gene were used to construct transcriptional-fusion mutants. One mutant susceptible to penicillin-induced killing (LMI2) and three\n         penicillin-tolerant derivatives (LMI103, LMI104, and LMI105) producing luciferase under independent streptococcal promoters were tested. The correlation between antibiotic-induced killing and luminescence\n         was determined with mechanistically unrelated drugs. Chloramphenicol (20 times the MIC) inhibited bacterial growth. In parallel, luciferase stopped increasing and remained stable, as determined by luminescence\n         and Western blots. Ciprofloxacin (200 times the MIC) rapidly killed 1.5 log\n                    <jats:sub>10<\/jats:sub>\n                    CFU\/ml in 2-4 hr. Luminescence decreased simultaneously by 10-fold. In contrast, penicillin (200 times the MIC) gave\n         discordant results. Although killing was slow (\u22640.5 log\n                    <jats:sub>10<\/jats:sub>\n                    CFU\/ml in 2 hr), luminescence dropped abruptly by 50-100-times in the same time. Inactivating penicillin with penicillinase restored\n         luminescence, irrespective of viable counts. This was not due to altered luciferase expression or stability, suggesting some kind of post-translational modification. Luciferase shares homology with aminoacyl-tRNA\n         synthetase and acyl-CoA ligase, which might be regulated by macromolecule synthesis and hence affected in penicillin-inhibited cells. Because of resemblance, luciferase might be down-regulated simultaneously.\n         Luminescence cannot be universally used to predict antibiotic-induced killing. Thus, introducing reporter enzymes sharing mechanistic similarities with normal metabolic reactions might reveal other effects\n         than those expected.\n                  <\/jats:p>","DOI":"10.1089\/107662903765826705","type":"journal-article","created":{"date-parts":[[2003,6,13]],"date-time":"2003-06-13T17:11:31Z","timestamp":1055524291000},"page":"123-131","source":"Crossref","is-referenced-by-count":15,"title":["Antibiotic-Dependent Correlation Between Drug-Induced Killing and Loss of Luminescence in\n                    <i>Streptococcus gordonii<\/i>\n                    Expressing Luciferase"],"prefix":"10.1177","volume":"9","author":[{"given":"B.","family":"Loeliger","sequence":"first","affiliation":[{"name":"Division of Infectious Diseases, Department of Internal Medicine, Centre Hospitalier Universitaire Vaudois, 1011 Lausanne, Switzerland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"I.","family":"Caldelari","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A.","family":"Bizzini","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"P. Stutzmann","family":"Meier","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"P.A.","family":"Majcherczyk","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"P.","family":"Moreillon","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[2003,6]]},"container-title":["Microbial Drug Resistance"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/journals.sagepub.com\/doi\/pdf\/10.1089\/107662903765826705","content-type":"application\/pdf","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/journals.sagepub.com\/doi\/pdf\/10.1089\/107662903765826705","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2026,2,10]],"date-time":"2026-02-10T18:14:14Z","timestamp":1770747254000},"score":1,"resource":{"primary":{"URL":"https:\/\/journals.sagepub.com\/doi\/full\/10.1089\/107662903765826705"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2003,6]]},"references-count":0,"journal-issue":{"issue":"2","published-print":{"date-parts":[[2003,6]]}},"alternative-id":["10.1089\/107662903765826705"],"URL":"https:\/\/doi.org\/10.1089\/107662903765826705","relation":{},"ISSN":["1076-6294","1931-8448"],"issn-type":[{"value":"1076-6294","type":"print"},{"value":"1931-8448","type":"electronic"}],"subject":[],"published":{"date-parts":[[2003,6]]}}}