{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,9]],"date-time":"2026-09-09T15:20:38Z","timestamp":1788967238912,"version":"build-2803163510"},"reference-count":69,"publisher":"American Society for Microbiology","license":[{"start":{"date-parts":[[2026,9,9]],"date-time":"2026-09-09T00:00:00Z","timestamp":1788912000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,9,9]],"date-time":"2026-09-09T00:00:00Z","timestamp":1788912000000},"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":["J Bacteriol"],"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title\/>\n                    <jats:p>\n                      The genus\n                      <jats:italic toggle=\"yes\">Acinetobacter<\/jats:italic>\n                      possesses non-canonical genes and responses to DNA damage. It encodes no LexA homolog to repress the ~150 SOS genes induced after exposure to various DNA-damaging agents, but two SOS regulators, UmuDAb and DdrR, repress both themselves and error-prone polymerases that generate mutations after DNA damage. Further differences include the lack of the Gram-negative cell division inhibitor (CDI), SulA, in members of the\n                      <jats:italic toggle=\"yes\">Moraxellaceae<\/jats:italic>\n                      family to which\n                      <jats:italic toggle=\"yes\">Acinetobacter<\/jats:italic>\n                      belongs. However,\n                      <jats:italic toggle=\"yes\">ddrR<\/jats:italic>\n                      , which lacks homologs outside the\n                      <jats:italic toggle=\"yes\">Acinetobacter<\/jats:italic>\n                      genus, is transcribed divergently from\n                      <jats:italic toggle=\"yes\">umuDAb<\/jats:italic>\n                      , like small CDIs of Gram-positive species lacking SulA, leading us to explore the possibility that DdrR inhibited cell division after DNA damage in the opportunistic\n                      <jats:italic toggle=\"yes\">Acinetobacter baumannii<\/jats:italic>\n                      . Like\n                      <jats:italic toggle=\"yes\">lexA<\/jats:italic>\n                      mutants of\n                      <jats:italic toggle=\"yes\">Escherichia coli<\/jats:italic>\n                      and\n                      <jats:italic toggle=\"yes\">Caulobacter crescentus<\/jats:italic>\n                      that overexpress CDIs SulA and SidA, respectively, a null\n                      <jats:italic toggle=\"yes\">umuDAb<\/jats:italic>\n                      mutant that overexpresses\n                      <jats:italic toggle=\"yes\">ddrR<\/jats:italic>\n                      formed filaments in the absence of DNA damage and further increased its cell length after DNA damage. A strain expressing a non-cleavable UmuDAb showed neither of these phenotypes, implicating a UmuDAb-repressed gene in the inhibition of cell division. However, \u0394\n                      <jats:italic toggle=\"yes\">umuDAb<\/jats:italic>\n                      \u0394\n                      <jats:italic toggle=\"yes\">ddrR<\/jats:italic>\n                      double mutant cells regained a wild-type cell length and did not form filaments after DNA damage, and\n                      <jats:italic toggle=\"yes\">ddrR<\/jats:italic>\n                      mutant cells had an impaired filamentation response to DNA damage relative to wild type. Conversely, wild-type cells overexpressing\n                      <jats:italic toggle=\"yes\">ddrR<\/jats:italic>\n                      became filamented in the absence of DNA damage.\n                      <jats:italic toggle=\"yes\">umuDAb<\/jats:italic>\n                      mutant cells overexpressing\n                      <jats:italic toggle=\"yes\">ddrR<\/jats:italic>\n                      exhibited impaired growth as measured by increased doubling times, lower optical density, and reduced cell viability. The rescue of these growth impairments by\n                      <jats:italic toggle=\"yes\">ddrR<\/jats:italic>\n                      mutation suggested that DdrR functions as a CDI in the DNA damage response of\n                      <jats:italic toggle=\"yes\">Acinetobacter<\/jats:italic>\n                      .\n                    <\/jats:p>\n                    <jats:sec>\n                      <jats:title>IMPORTANCE<\/jats:title>\n                      <jats:p>\n                        In hospital environments, the multi-drug-resistant opportunistic pathogen\n                        <jats:italic toggle=\"yes\">Acinetobacter baumannii<\/jats:italic>\n                        incurs DNA damage from antibiotics, UV exposure, and desiccation, which induces multiple error-prone polymerases that can cause clinically relevant antibiotic resistance. However, while\n                        <jats:italic toggle=\"yes\">Acinetobacter<\/jats:italic>\n                        species lack the common DNA damage response proteins LexA and SulA, they also show the typical DNA damage response of a cell division checkpoint. We found that the small SOS protein DdrR inhibited cell division like Gram-positive cell division inhibitor (CDI) proteins. After DNA damage, DdrR was required for the cell filamentation response, while increased DdrR expression impaired cell growth and viability. Uncovering a novel mechanism of controlling growth inhibition after DNA damage presents an opportunity to define a new model of inhibiting cell division for non-\n                        <jats:italic toggle=\"yes\">Enterobacteriaceae<\/jats:italic>\n                        Gram-negative Gammaproteobacteria.\n                      <\/jats:p>\n                    <\/jats:sec>\n                  <\/jats:sec>","DOI":"10.1128\/jb.00416-26","type":"journal-article","created":{"date-parts":[[2026,9,9]],"date-time":"2026-09-09T14:44:35Z","timestamp":1788965075000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":0,"title":["DdrR acts as a DNA damage-induced cell division inhibitor in\n                    <i>Acinetobacter baumannii<\/i>"],"prefix":"10.1128","author":[{"given":"Christian P.","family":"Lowe","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/018yta094","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Biology and Chemistry, Morehead State University","place":["Morehead, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Deborah","family":"Cook","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/018yta094","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Biology and Chemistry, Morehead State University","place":["Morehead, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lily","family":"Hoard","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/018yta094","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Biology and Chemistry, Morehead State University","place":["Morehead, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"McKinnley","family":"Martin","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/018yta094","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Biology and Chemistry, Morehead State University","place":["Morehead, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5482-8143","authenticated-orcid":true,"given":"Janelle M.","family":"Hare","sequence":"additional","affiliation":[{"id":[{"id":"https:\/\/ror.org\/018yta094","id-type":"ROR","asserted-by":"publisher"}],"name":"Department of Biology and Chemistry, Morehead State University","place":["Morehead, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","published-online":{"date-parts":[[2026,9,9]]},"reference":[{"key":"e_1_3_4_2_2","doi-asserted-by":"publisher","DOI":"10.1002\/em.22267"},{"key":"e_1_3_4_3_2","doi-asserted-by":"publisher","DOI":"10.1146\/annurev.genet.34.1.479"},{"key":"e_1_3_4_4_2","doi-asserted-by":"publisher","DOI":"10.1016\/s0921-8777(00)00076-8"},{"key":"e_1_3_4_5_2","volume-title":"The SOS response of Escherichia coli","author":"Walker GC","year":"1996","unstructured":"Walker GC. 1996. 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