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Here, we address this question by examining the role of regulated variations in <jats:styled-content style=\"fixed-case\">O<\/jats:styled-content>\u2010antigen length in the lipopolysaccharide (<jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content>), a glycolipid that forms most of the outer leaflet of the outer membrane in Gram\u2010negative bacteria. We determined that activation of the <jats:styled-content style=\"fixed-case\">PmrA<\/jats:styled-content>\/<jats:styled-content style=\"fixed-case\">PmrB<\/jats:styled-content> two\u2010component system, which is the major regulator of <jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content> alterations in <jats:italic><jats:styled-content style=\"fixed-case\">S<\/jats:styled-content>almonella enterica<\/jats:italic> serovar <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>yphimurium, impaired growth of <jats:italic><jats:styled-content style=\"fixed-case\">S<\/jats:styled-content>almonella<\/jats:italic> in bile. This growth defect required the <jats:styled-content style=\"fixed-case\">PmrA<\/jats:styled-content>\u2010activated gene <jats:styled-content style=\"fixed-case\"><jats:italic>wzz<\/jats:italic><\/jats:styled-content><jats:sub>st<\/jats:sub>, which encodes the protein that determines long <jats:styled-content style=\"fixed-case\">O<\/jats:styled-content>\u2010antigen chain length and confers resistance to complement\u2010mediated killing. By contrast, this growth defect did not require the <jats:styled-content style=\"fixed-case\"><jats:italic>wzz<\/jats:italic><\/jats:styled-content><jats:sub>fepE<\/jats:sub> gene, which controls production of very long <jats:styled-content style=\"fixed-case\">O<\/jats:styled-content>\u2010antigen, or other <jats:styled-content style=\"fixed-case\">PmrA<\/jats:styled-content>\u2010activated genes that mediate modifications of lipid <jats:styled-content style=\"fixed-case\">A<\/jats:styled-content> or core regions of the <jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content>. Additionally, we establish that long <jats:styled-content style=\"fixed-case\">O<\/jats:styled-content>\u2010antigen inhibits growth in bile only in the presence of enterobacterial common antigen, an outer\u2010membrane glycolipid that contributes to bile resistance. Our results suggest that <jats:italic><jats:styled-content style=\"fixed-case\">S<\/jats:styled-content>almonella<\/jats:italic> regulates the proportion of long <jats:styled-content style=\"fixed-case\">O<\/jats:styled-content>\u2010antigen in its <jats:styled-content style=\"fixed-case\">LPS<\/jats:styled-content> to respond to the different conditions it faces during infection.<\/jats:p>","DOI":"10.1111\/mmi.12236","type":"journal-article","created":{"date-parts":[[2013,5,6]],"date-time":"2013-05-06T04:09:43Z","timestamp":1367813383000},"page":"970-983","source":"Crossref","is-referenced-by-count":27,"title":["Conflicting roles for a cell surface modification in <i><scp>S<\/scp>almonella<\/i>"],"prefix":"10.1111","volume":"88","author":[{"given":"John F.","family":"May","sequence":"first","affiliation":[{"name":"Department of Microbial Pathogenesis Yale School of Medicine  New Haven CT 06536 USA"},{"name":"Yale Microbial Diversity Institute  West Haven CT 06516 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