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The closely related\n            <jats:italic>Yersinia pseudotuberculosis<\/jats:italic>\n            , from which\n            <jats:italic>Y. pestis<\/jats:italic>\n            recently evolved, can colonize the flea midgut but does not form a biofilm in the foregut.\n            <jats:italic>Y. pestis<\/jats:italic>\n            biofilm in the flea and in vitro is dependent on an extracellular matrix synthesized by products of the\n            <jats:italic>hms<\/jats:italic>\n            genes; identical genes are present in\n            <jats:italic>Y. pseudotuberculosis<\/jats:italic>\n            . The\n            <jats:italic>Yersinia<\/jats:italic>\n            Hms proteins contain functional domains present in\n            <jats:italic>Escherichia coli<\/jats:italic>\n            and\n            <jats:italic>Staphylococcus<\/jats:italic>\n            proteins known to synthesize a poly-\u03b2-1,6-\n            <jats:italic>N<\/jats:italic>\n            -acetyl-\n            <jats:sc>d<\/jats:sc>\n            -glucosamine biofilm matrix. In this study, we show that the extracellular matrices (ECM) of\n            <jats:italic>Y. pestis<\/jats:italic>\n            and staphylococcal biofilms are antigenically related, indicating a similar biochemical structure. We also characterized a glycosyl hydrolase (NghA) of\n            <jats:italic>Y. pseudotuberculosis<\/jats:italic>\n            that cleaved \u03b2-linked\n            <jats:italic>N<\/jats:italic>\n            -acetylglucosamine residues and reduced biofilm formation by staphylococci and\n            <jats:italic>Y. pestis<\/jats:italic>\n            in vitro. The\n            <jats:italic>Y. pestis nghA<\/jats:italic>\n            ortholog is a pseudogene, and overexpression of functional\n            <jats:italic>nghA<\/jats:italic>\n            reduced ECM surface accumulation and inhibited the ability of\n            <jats:italic>Y. pestis<\/jats:italic>\n            to produce biofilm in the flea foregut. Mutational loss of this glycosidase activity in\n            <jats:italic>Y. pestis<\/jats:italic>\n            may have contributed to the recent evolution of flea-borne transmission.\n          <\/jats:p>","DOI":"10.1128\/jb.01181-08","type":"journal-article","created":{"date-parts":[[2008,10,18]],"date-time":"2008-10-18T00:59:46Z","timestamp":1224291586000},"page":"8163-8170","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":51,"title":["Loss of a Biofilm-Inhibiting Glycosyl Hydrolase during the Emergence of\n            <i>Yersinia pestis<\/i>"],"prefix":"10.1128","volume":"190","author":[{"given":"David L.","family":"Erickson","sequence":"first","affiliation":[{"name":"Laboratory of Zoonotic Pathogens"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Clayton O.","family":"Jarrett","sequence":"additional","affiliation":[{"name":"Laboratory of Zoonotic Pathogens"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Julie A.","family":"Callison","sequence":"additional","affiliation":[{"name":"Laboratory of Zoonotic Pathogens"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elizabeth R.","family":"Fischer","sequence":"additional","affiliation":[{"name":"RTS Microscopy Unit, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 903 S. 4th St., Hamilton, Montana 59840"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"B. 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