{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,8]],"date-time":"2026-04-08T02:16:36Z","timestamp":1775614596496,"version":"3.50.1"},"reference-count":57,"publisher":"American Society for Microbiology","issue":"6","license":[{"start":{"date-parts":[[2016,6,1]],"date-time":"2016-06-01T00:00:00Z","timestamp":1464739200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"funder":[{"DOI":"10.13039\/100000002","name":"HHS | National Institutes of Health","doi-asserted-by":"publisher","award":["R01AI063517"],"award-info":[{"award-number":["R01AI063517"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"HHS | National Institutes of Health","doi-asserted-by":"publisher","award":["R01AI72219"],"award-info":[{"award-number":["R01AI72219"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"HHS | National Institutes of Health","doi-asserted-by":"publisher","award":["R01AI100560"],"award-info":[{"award-number":["R01AI100560"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Antimicrob Agents Chemother"],"published-print":{"date-parts":[[2016,6]]},"abstract":"ABSTRACT<\/jats:title>\n \n Transposon mutagenesis was used to identify novel determinants of intrinsic \u03b2-lactam resistance in\n Acinetobacter baumannii<\/jats:named-content>\n . An EZ-Tn5 transposon insertion in a gene corresponding to the A1S_0225 sequence resulted in a 4-fold decrease in resistance to ampicillin, cefotaxime, imipenem, and ceftriaxone but did not alter resistance to other classes of antibiotics. Based on this phenotype, the gene was designated\n blhA<\/jats:italic>\n (\n \u03b2<\/jats:underline>\n -\n l<\/jats:underline>\n actam\n h<\/jats:underline>\n ypersusceptibility). The\n blhA<\/jats:italic>\n ::EZ-Tn5 mutation conferred a similar phenotype in\n A. baumannii<\/jats:named-content>\n strain ATCC 17978. The wild-type\n blhA<\/jats:italic>\n gene complemented the\n blhA<\/jats:italic>\n ::EZTn5 insertion and restored \u03b2-lactam resistance levels back to wild-type levels. The\n blhA<\/jats:italic>\n mutation also increased \u03b2-lactam susceptibility in an\n adeB adeJ<\/jats:italic>\n double mutant, indicating that the\n blhA<\/jats:italic>\n mutation acted independently of these efflux systems to mediate susceptibility. In addition, mRNA levels for the\n bla<\/jats:italic>\n OXA<\/jats:sub>\n and\n bla<\/jats:italic>\n ADC<\/jats:sub>\n \u03b2-lactamase genes were not altered by the\n blhA<\/jats:italic>\n mutation. The\n blhA<\/jats:italic>\n mutation resulted in a prominent cell division and morphological defect, with cells exhibiting a highly elongated phenotype, combined with large bulges in some cells. The\n blhA<\/jats:italic>\n gene is unique to\n Acinetobacter<\/jats:named-content>\n and likely represents a novel gene involved in cell division. Three additional mutations, in\n zipA<\/jats:italic>\n ,\n zapA<\/jats:italic>\n , and\n ftsK<\/jats:italic>\n , each of which encode predicted cell division proteins, also conferred increased \u03b2-lactam susceptibility, indicating a common link between cell division and intrinsic \u03b2-lactam resistance in\n A. baumannii<\/jats:named-content>\n .\n <\/jats:p>","DOI":"10.1128\/aac.00361-16","type":"journal-article","created":{"date-parts":[[2016,4,12]],"date-time":"2016-04-12T03:39:01Z","timestamp":1460432341000},"page":"3751-3758","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":26,"title":["Mutations Decreasing Intrinsic \u03b2-Lactam Resistance Are Linked to Cell Division in the Nosocomial Pathogen Acinetobacter baumannii"],"prefix":"10.1128","volume":"60","author":[{"given":"Daniel","family":"Knight","sequence":"first","affiliation":[{"name":"Research Service, Veterans Affairs Medical Center, Decatur, Georgia, 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