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Upon infecting a host cell,\n                    <jats:named-content content-type=\"genus-species\">L. monocytogenes<\/jats:named-content>\n                    upregulates the transcription of numerous factors necessary for productive infection. VirR is the response regulator component of a two-component regulatory system in\n                    <jats:named-content content-type=\"genus-species\">L. monocytogenes<\/jats:named-content>\n                    . In this report, we have identified the putative ABC transporter encoded by genes\n                    <jats:italic>lmo1746-lmo1747<\/jats:italic>\n                    as necessary for VirR function. We have designated\n                    <jats:italic>lmo1746-lmo1747 virAB<\/jats:italic>\n                    . We constructed an in-frame deletion of\n                    <jats:italic>virAB<\/jats:italic>\n                    and determined that the \u0394\n                    <jats:italic>virAB<\/jats:italic>\n                    mutant exhibited reduced transcription of VirR-regulated genes. The \u0394\n                    <jats:italic>virAB<\/jats:italic>\n                    mutant also showed defects in\n                    <jats:italic>in vitro<\/jats:italic>\n                    plaque formation and\n                    <jats:italic>in vivo<\/jats:italic>\n                    virulence that were similar to those of a \u0394\n                    <jats:italic>virR<\/jats:italic>\n                    deletion mutant. Since VirR is important for innate resistance to antimicrobial agents, we determined the MICs of nisin and bacitracin for \u0394\n                    <jats:italic>virAB<\/jats:italic>\n                    bacteria. We found that VirAB expression was necessary for nisin resistance but was dispensable for resistance to bacitracin. This result suggested a VirAB-independent mechanism of VirR regulation in response to bacitracin. Lastly, we found that the \u0394\n                    <jats:italic>virR<\/jats:italic>\n                    and \u0394\n                    <jats:italic>virAB<\/jats:italic>\n                    mutants had no deficiency in growth in broth culture, intracellular replication, or production of the ActA surface protein, which facilitates actin-based motility and cell-to-cell spread. However, the \u0394\n                    <jats:italic>virR<\/jats:italic>\n                    and \u0394\n                    <jats:italic>virAB<\/jats:italic>\n                    mutants produced shorter actin tails during intracellular infection, which suggested that these mutants have a reduced ability to move and spread via actin-based motility. These findings have demonstrated that\n                    <jats:named-content content-type=\"genus-species\">L. monocytogenes<\/jats:named-content>\n                    VirAB functions in a pathway with VirR to regulate the expression of genes necessary for virulence and resistance to antimicrobial agents.\n                  <\/jats:p>","DOI":"10.1128\/iai.00901-17","type":"journal-article","created":{"date-parts":[[2017,12,21]],"date-time":"2017-12-21T08:11:39Z","timestamp":1513843899000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":53,"title":["The VirAB ABC Transporter Is Required for VirR Regulation of Listeria monocytogenes Virulence and Resistance to Nisin"],"prefix":"10.1128","volume":"86","author":[{"given":"Daniel","family":"Grubaugh","sequence":"first","affiliation":[{"name":"Department of Microbiology and Immunobiology, Harvard Medical School, Boston, Massachusetts, 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