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However, the mechanism by which<jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">Y. pestis<\/jats:named-content>promotes its intracellular survival is not well understood. To identify genes that are important for<jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">Y. pestis<\/jats:named-content>survival in macrophages, a library comprised of \u223c31,500<jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">Y. pestis<\/jats:named-content>KIM6+ transposon insertion mutants (input pool) was subjected to negative selection in primary murine macrophages. Genes underrepresented in the output pool of surviving bacteria were identified by transposon site hybridization to DNA oligonucleotide microarrays. The screen identified several genes known to be important for survival of<jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">Y. pestis<\/jats:named-content>in macrophages, including<jats:italic>phoPQ<\/jats:italic>and members of the PhoPQ regulon (e.g.,<jats:italic>pmrF<\/jats:italic>). In addition, genes predicated to encode a glucose-1-phosphate uridylyltransferase (<jats:italic>galU<\/jats:italic>), a UDP-<jats:italic>N<\/jats:italic>-acetylglucosamine 2-epimerase (<jats:italic>wecB<\/jats:italic>) and a UDP-<jats:italic>N<\/jats:italic>-acetyl-<jats:sc>d<\/jats:sc>-mannosamine dehydrogenase (<jats:italic>wecC<\/jats:italic>) were identified in the screen. Viable-count assays demonstrated that a KIM6+<jats:italic>galU<\/jats:italic>mutant and a KIM6+<jats:italic>wecBC<\/jats:italic>mutant were defective for survival in murine macrophages. The<jats:italic>galU<\/jats:italic>mutant was studied further because of its strong phenotype. The KIM6+<jats:italic>galU<\/jats:italic>mutant exhibited increased susceptibility to the antimicrobial peptides polymyxin B and cathelicidin-related antimicrobial peptide (CRAMP). Polyacrylamide gel electrophoresis demonstrated that the lipooligosaccharide (LOS) of the<jats:italic>galU<\/jats:italic>mutant migrated faster than the LOS of the parent KIM6+, suggesting the core was truncated. In addition, the analysis of LOS isolated from the<jats:italic>galU<\/jats:italic>mutant by mass spectrometry showed that aminoarabinose modification of lipid A is absent. Therefore, addition of aminoarabinose to lipid A and complete LOS core (<jats:italic>galU<\/jats:italic>), as well as enterobacterial common antigen (<jats:italic>wecB<\/jats:italic>and<jats:italic>wecC<\/jats:italic>), is important for survival of<jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">Y. pestis<\/jats:named-content>in macrophages.<\/jats:p>","DOI":"10.1128\/jb.06237-11","type":"journal-article","created":{"date-parts":[[2011,12,3]],"date-time":"2011-12-03T20:25:32Z","timestamp":1322943932000},"page":"653-662","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":38,"title":["A Transposon Site Hybridization Screen Identifies<i>galU<\/i>and<i>wecBC<\/i>as Important for Survival of Yersinia pestis in Murine Macrophages"],"prefix":"10.1128","volume":"194","author":[{"given":"Kathryn A.","family":"Klein","sequence":"first","affiliation":[{"name":"Center for Infectious Diseases and Department of Molecular Genetics and Microbiology, Stony Brook University, Stony Brook, New York, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hana S.","family":"Fukuto","sequence":"additional","affiliation":[{"name":"Center for Infectious Diseases and Department of Molecular Genetics and Microbiology, Stony Brook University, Stony Brook, New York, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mark","family":"Pelletier","sequence":"additional","affiliation":[{"name":"Department of Microbial Pathogenesis, University of Maryland\u2014Baltimore, School of Dentistry, Baltimore, Maryland, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Galina","family":"Romanov","sequence":"additional","affiliation":[{"name":"Center for Infectious Diseases and Department of Molecular Genetics and Microbiology, Stony Brook University, Stony Brook, New York, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jens P.","family":"Grabenstein","sequence":"additional","affiliation":[{"name":"Center for Infectious Diseases and Department of Molecular Genetics and Microbiology, Stony Brook University, Stony Brook, New York, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lance E.","family":"Palmer","sequence":"additional","affiliation":[{"name":"Center for Infectious Diseases and Department of Molecular Genetics and Microbiology, Stony Brook University, Stony Brook, New York, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Robert","family":"Ernst","sequence":"additional","affiliation":[{"name":"Department of Microbial Pathogenesis, University of Maryland\u2014Baltimore, School of Dentistry, Baltimore, Maryland, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"James B.","family":"Bliska","sequence":"additional","affiliation":[{"name":"Center for Infectious Diseases and Department of Molecular Genetics and Microbiology, Stony Brook University, Stony Brook, New York, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0408026101"},{"key":"e_1_3_3_3_2","volume-title":"The challenge of highly pathogenic microorganisms: Mechanisms of virulence and novel medical countermeasures","author":"Anisimov AP","year":"2010","unstructured":"AnisimovAP. 2010. 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