{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,24]],"date-time":"2026-09-24T09:16:08Z","timestamp":1790241368543,"version":"4.1.0"},"reference-count":27,"publisher":"American Society for Microbiology","issue":"11","license":[{"start":{"date-parts":[[2006,11,1]],"date-time":"2006-11-01T00:00:00Z","timestamp":1162339200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Antimicrob Agents Chemother"],"published-print":{"date-parts":[[2006,11]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Bacterial genes defining intrinsic resistance to antibiotics encode proteins that can be targeted by antibiotic potentiators. To find such genes, a transposon insertion library of\n                    <jats:italic>Acinetobacter baylyi<\/jats:italic>\n                    was screened with subinhibitory concentrations of various antibiotics to find supersusceptible mutants. A DNA microarray printer was used to replica plate 10,000 individual library clones to select mutants unable to grow at 1\/10 the MICs of 12 different antibiotics. Transposon insertions in 11 genes were found to cause an eightfold or higher hypersusceptibility to at least one antibiotic. Most of the mutants identified exhibited hypersusceptibility to \u03b2-lactam antibiotics. These included mutants with disruptions of genes encoding proteins involved in efflux (\n                    <jats:italic>acrB<\/jats:italic>\n                    and\n                    <jats:italic>oprM<\/jats:italic>\n                    ) as well as genes pertaining to peptidoglycan synthesis and modification (\n                    <jats:italic>ampD<\/jats:italic>\n                    ,\n                    <jats:italic>mpl<\/jats:italic>\n                    , and\n                    <jats:italic>pbpG<\/jats:italic>\n                    ). However, disruptions of genes encoding proteins with seemingly unrelated functions (\n                    <jats:italic>gph<\/jats:italic>\n                    ,\n                    <jats:italic>argH<\/jats:italic>\n                    ,\n                    <jats:italic>hisF, and ACIAD0795<\/jats:italic>\n                    ) can also render cells hypersusceptible to \u03b2-lactam antibiotics. A knockout of\n                    <jats:italic>gshA<\/jats:italic>\n                    , involved in glutathione biosynthesis, enhanced the susceptibility to metronidazole, while a knockout of\n                    <jats:italic>recD<\/jats:italic>\n                    , involved in recombination and repair, made the bacteria hypersusceptible to ciprofloxacin. Disruption of\n                    <jats:italic>acrB<\/jats:italic>\n                    in\n                    <jats:italic>Escherichia coli<\/jats:italic>\n                    rendered the cells hypersusceptible to several antibiotics. However, knockout mutants of other homologous genes in\n                    <jats:italic>E. coli<\/jats:italic>\n                    showed no significant changes in antibiotic MICs, indicating that the intrinsic resistance genes are species specific.\n                  <\/jats:p>","DOI":"10.1128\/aac.00579-06","type":"journal-article","created":{"date-parts":[[2006,10,25]],"date-time":"2006-10-25T16:58:50Z","timestamp":1161795530000},"page":"3562-3567","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":81,"title":["Genes Involved in Intrinsic Antibiotic Resistance of\n                    <i>Acinetobacter baylyi<\/i>"],"prefix":"10.1128","volume":"50","author":[{"given":"Maria J.","family":"Gomez","sequence":"first","affiliation":[{"name":"Center for Pharmaceutical Biotechnology, University of Illinois, Chicago, Illinois 60607"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alexander A.","family":"Neyfakh","sequence":"additional","affiliation":[{"name":"Center for Pharmaceutical Biotechnology, University of Illinois, Chicago, Illinois 60607"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"crossref","first-page":"5558","DOI":"10.1073\/pnas.83.15.5558","volume":"83","year":"1986","unstructured":"Amundsen, S. 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