{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,27]],"date-time":"2026-09-27T10:32:06Z","timestamp":1790505126263,"version":"4.1.0"},"reference-count":73,"publisher":"American Society for Microbiology","issue":"9","license":[{"start":{"date-parts":[[2015,9,1]],"date-time":"2015-09-01T00:00:00Z","timestamp":1441065600000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Infect Immun"],"published-print":{"date-parts":[[2015,9]]},"abstract":"ABSTRACT<\/jats:title>\n \n The\n opgGH<\/jats:italic>\n operon encodes glucosyltransferases that synthesize osmoregulated periplasmic glucans (OPGs) from UDP-glucose, using acyl carrier protein (ACP) as a cofactor. OPGs are required for motility, biofilm formation, and virulence in various bacteria. OpgH also sequesters FtsZ in order to regulate cell size according to nutrient availability.\n Yersinia pestis<\/jats:named-content>\n (the agent of flea-borne plague) lost the\n opgGH<\/jats:italic>\n operon during its emergence from the enteropathogen\n Yersinia pseudotuberculosis<\/jats:named-content>\n . When expressed in OPG-negative strains of\n Escherichia coli<\/jats:named-content>\n and\n Dickeya dadantii<\/jats:italic>\n ,\n opgGH<\/jats:italic>\n from\n Y. pseudotuberculosis<\/jats:named-content>\n restored OPGs synthesis, motility, and virulence. However,\n Y. pseudotuberculosis<\/jats:named-content>\n did not produce OPGs (i) under various growth conditions or (ii) when overexpressing its\n opgGH<\/jats:italic>\n operon, its\n galUF<\/jats:italic>\n operon (governing UDP-glucose), or the\n opgGH<\/jats:italic>\n operon or Acp from\n E. coli<\/jats:named-content>\n . A \u0394\n opgGH<\/jats:italic>\n Y. pseudotuberculosis<\/jats:named-content>\n strain showed normal motility, biofilm formation, resistance to polymyxin and macrophages, and virulence but was smaller. Consistently,\n Y. pestis<\/jats:named-content>\n was smaller than\n Y. pseudotuberculosis<\/jats:named-content>\n when cultured at \u226537\u00b0C, except when the plague bacillus expressed\n opgGH<\/jats:italic>\n .\n Y. pestis<\/jats:named-content>\n expressing\n opgGH<\/jats:italic>\n grew normally in serum and within macrophages and was fully virulent in mice, suggesting that small cell size was not advantageous in the mammalian host. Lastly,\n Y. pestis<\/jats:named-content>\n expressing\n opgGH<\/jats:italic>\n was able to infect\n Xenopsylla cheopis<\/jats:named-content>\n fleas normally. Our results suggest an evolutionary scenario whereby an ancestral\n Yersinia<\/jats:named-content>\n strain lost a factor required for OPG biosynthesis but kept\n opgGH<\/jats:italic>\n (to regulate cell size). The\n opgGH<\/jats:italic>\n operon was presumably then lost because OpgH-dependent cell size control became unnecessary.\n <\/jats:p>","DOI":"10.1128\/iai.00482-15","type":"journal-article","created":{"date-parts":[[2015,7,7]],"date-time":"2015-07-07T02:30:36Z","timestamp":1436236236000},"page":"3638-3647","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":18,"title":["Evaluation of the Role of the\n opgGH<\/i>\n Operon in Yersinia pseudotuberculosis and Its Deletion during the Emergence of Yersinia pestis"],"prefix":"10.1128","volume":"83","author":[{"given":"K\u00e9vin","family":"Quintard","sequence":"first","affiliation":[{"name":"Plague and Yersinia pestis Group, INSERM U1019, Lille, France"},{"name":"Centre National de la Recherche Scientifique UMR8204, Lille, France"},{"name":"Institut Pasteur de Lille, Centre d'Infection et d'Immunit\u00e9 de Lille, Lille, France"},{"name":"Universit\u00e9 Lille Nord de France, 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