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In\n \n E<\/jats:italic>\n <\/jats:styled-content>\n scherichia coli<\/jats:italic>\n , mutants lacking these proteins often have no phenotype, and cells lacking all seven\n LMW PBPs<\/jats:styled-content>\n remain viable. In contrast, we report here that\n \n V<\/jats:italic>\n <\/jats:styled-content>\n ibrio cholerae<\/jats:italic>\n lacking\n DacA<\/jats:styled-content>\n \u20101, a\n PBP<\/jats:styled-content>\n 5 homologue, displays slow growth, aberrant morphology and altered peptidoglycan (\n PG<\/jats:styled-content>\n ) homeostasis in Luria\u2013Bertani (\n LB<\/jats:styled-content>\n ) medium, as well as a profound plating defect.\n DacA<\/jats:styled-content>\n \u20101 alone among\n \n V<\/jats:italic>\n <\/jats:styled-content>\n .\u2009cholerae's<\/jats:italic>\n \u2005\n LMW PBPs<\/jats:styled-content>\n is critical for bacterial growth; mutants lacking the related protein\n DacA<\/jats:styled-content>\n \u20102 and\/or homologues of\n PBP<\/jats:styled-content>\n 4 or\n PBP<\/jats:styled-content>\n 7 displayed normal growth and morphology. Remarkably, the growth and morphology of the\n dac<\/jats:italic>\n \n A<\/jats:italic>\n <\/jats:styled-content>\n \u20101<\/jats:italic>\n mutant were unimpaired in\n LB<\/jats:styled-content>\n media containing reduced concentrations of\n N<\/jats:styled-content>\n a\n C<\/jats:styled-content>\n l (100\u2009mM or less), and also within suckling mice, a model host for the study of cholera pathogenesis. Peptidoglycan from the\n dac<\/jats:italic>\n \n A<\/jats:italic>\n <\/jats:styled-content>\n \u20101<\/jats:italic>\n mutant contained elevated pentapeptide levels in standard and low salt media, and comparative analyses suggest that\n DacA<\/jats:styled-content>\n \u20101 is\n \n V<\/jats:italic>\n <\/jats:styled-content>\n .\u2009cholerae's<\/jats:italic>\n principal\n DD<\/jats:styled-content>\n \u2010carboxypeptidase. The basis for the\n dac<\/jats:italic>\n \n A<\/jats:italic>\n <\/jats:styled-content>\n \u20101<\/jats:italic>\n mutant's halosensitivity is unknown; nonetheless, the mutant's survival in biochemically uncharacterized environments (such as the suckling mouse intestine) can be used as a reporter of low\n N<\/jats:styled-content>\n a\n +<\/jats:sup>\n content.\n <\/jats:p>","DOI":"10.1111\/1462-2920.12779","type":"journal-article","created":{"date-parts":[[2015,1,29]],"date-time":"2015-01-29T06:53:22Z","timestamp":1422514402000},"page":"527-540","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":41,"title":["A\n D<\/scp>\n ,\n D<\/scp>\n \u2010carboxypeptidase is required for\n \n V<\/i>\n <\/scp>\n ibrio cholerae<\/i>\n halotolerance"],"prefix":"10.1111","volume":"17","author":[{"given":"Andrea","family":"M\u00f6ll","sequence":"first","affiliation":[{"name":"Division of Infectious Diseases Brigham and Women's Hospital Boston MA 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