{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T08:11:34Z","timestamp":1790755894662,"version":"4.1.0"},"reference-count":20,"publisher":"National Academy of Sciences","issue":"22","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2004,6]]},"abstract":"<jats:p>\n                    Plague, the disease caused by the bacterium\n                    <jats:italic>Yersinia pestis<\/jats:italic>\n                    , has greatly impacted human civilization.\n                    <jats:italic>Y<\/jats:italic>\n                    .\n                    <jats:italic>pestis<\/jats:italic>\n                    is a successful global pathogen, with active foci on all continents except Australia and Antarctica. Because the\n                    <jats:italic>Y<\/jats:italic>\n                    .\n                    <jats:italic>pestis<\/jats:italic>\n                    genome is highly monomorphic, previous attempts to characterize the population genetic structure within a single focus have been largely unsuccessful. Here we report that highly mutable marker loci allow determination of\n                    <jats:italic>Y<\/jats:italic>\n                    .\n                    <jats:italic>pestis<\/jats:italic>\n                    population genetic structure and tracking of transmission patterns at two spatial scales within a single focus. In addition, we found that\n                    <jats:italic>in vitro<\/jats:italic>\n                    mutation rates for these loci are similar to those observed\n                    <jats:italic>in vivo<\/jats:italic>\n                    , which allowed us to develop a mutation-rate-based model to examine transmission mechanisms. Our model suggests there are two primary components of plague ecology: a rapid expansion phase for population growth and dispersal followed by a slower persistence phase. This pattern seems consistent across local, regional, and even global scales.\n                  <\/jats:p>","DOI":"10.1073\/pnas.0401561101","type":"journal-article","created":{"date-parts":[[2004,6,1]],"date-time":"2004-06-01T14:38:33Z","timestamp":1086100713000},"page":"8408-8413","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":112,"title":["Differential plague-transmission dynamics determine\n                    <i>Yersinia pestis<\/i>\n                    population genetic structure on local, regional, and global scales"],"prefix":"10.1073","volume":"101","author":[{"given":"Jessica M.","family":"Girard","sequence":"first","affiliation":[{"name":"Department of Biological Sciences, Northern Arizona University, Flagstaff, AZ 86011-5640; and Translational Genomics Research Institute, 400 North Fifth Street, Suite 1600, Phoenix, AZ 85004"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David M.","family":"Wagner","sequence":"additional","affiliation":[{"name":"Department of Biological Sciences, Northern Arizona University, Flagstaff, AZ 86011-5640; and Translational Genomics Research Institute, 400 North Fifth Street, Suite 1600, Phoenix, AZ 85004"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Amy J.","family":"Vogler","sequence":"additional","affiliation":[{"name":"Department of Biological Sciences, Northern Arizona University, Flagstaff, AZ 86011-5640; and Translational Genomics Research Institute, 400 North Fifth Street, Suite 1600, Phoenix, AZ 85004"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christine","family":"Keys","sequence":"additional","affiliation":[{"name":"Department of Biological Sciences, Northern Arizona University, Flagstaff, AZ 86011-5640; and Translational Genomics Research Institute, 400 North Fifth Street, Suite 1600, Phoenix, AZ 85004"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christopher J.","family":"Allender","sequence":"additional","affiliation":[{"name":"Department of Biological Sciences, Northern Arizona University, Flagstaff, AZ 86011-5640; and Translational Genomics Research Institute, 400 North Fifth Street, Suite 1600, Phoenix, AZ 85004"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lee C.","family":"Drickamer","sequence":"additional","affiliation":[{"name":"Department of Biological Sciences, Northern Arizona University, Flagstaff, AZ 86011-5640; and Translational Genomics Research Institute, 400 North Fifth Street, Suite 1600, Phoenix, AZ 85004"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paul","family":"Keim","sequence":"additional","affiliation":[{"name":"Department of Biological Sciences, Northern Arizona University, Flagstaff, AZ 86011-5640; and Translational Genomics Research Institute, 400 North Fifth Street, Suite 1600, Phoenix, AZ 85004"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"341","published-online":{"date-parts":[[2004,5,20]]},"reference":[{"key":"e_1_3_2_1_2","doi-asserted-by":"publisher","DOI":"10.1128\/CMR.10.1.35"},{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.96.4.1403"},{"key":"e_1_3_2_3_2","unstructured":"Poland J. 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