{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"institution":[{"name":"bioRxiv"}],"indexed":{"date-parts":[[2026,5,5]],"date-time":"2026-05-05T12:25:18Z","timestamp":1777983918412,"version":"3.51.4"},"posted":{"date-parts":[[2024,8,31]]},"group-title":"Evolutionary Biology","reference-count":128,"publisher":"openRxiv","license":[{"start":{"date-parts":[[2024,8,31]],"date-time":"2024-08-31T00:00:00Z","timestamp":1725062400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/www.biorxiv.org\/about\/FAQ#license"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"accepted":{"date-parts":[[2026,2,11]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                <jats:p>\n                  Widespread antibiotic usage has resulted in the rapid evolution of drug-resistant bacterial pathogens and poses significant threats to public health. Resolving how pathogens respond to antibiotics under different contexts is critical for understanding disease emergence and evolution going forward. The impact of antibiotics has been demonstrated most directly through\n                  <jats:italic>in vitro<\/jats:italic>\n                  pathogen passaging experiments. Independent from antibiotic selection, interactions with hosts have also altered the evolutionary trajectories and fitness landscapes of pathogens, shaping infectious disease outcomes. However, it is unclear how interactions between hosts and antibiotics impact the evolution of pathogen virulence. Here, we evolved and re-sequenced\n                  <jats:italic>Staphylococcus aureus,<\/jats:italic>\n                  a major bacterial pathogen, varying exposure to host and antibiotics to tease apart the contributions of these selective pressures on pathogen adaptation. After 12 passages,\n                  <jats:italic>S. aureus<\/jats:italic>\n                  evolving in\n                  <jats:italic>Caenorhabditis elegans<\/jats:italic>\n                  nematodes exposed to a sub-minimum inhibitory concentration of antibiotic (oxacillin) became highly virulent, regardless of whether the ancestral pathogen was methicillin-resistant (MRSA) or methicillin-sensitive (MSSA). Host and antibiotic exposure selected for reduced drug susceptibility in MSSA lineages while increasing MRSA total growth outside hosts. We identified mutations in genes involved in complex regulatory networks linking virulence and metabolism, including\n                  <jats:italic>codY<\/jats:italic>\n                  ,\n                  <jats:italic>agr<\/jats:italic>\n                  , and\n                  <jats:italic>gdpP<\/jats:italic>\n                  , suggesting that rapid adaptation to infect hosts may have pleiotropic effects. In particular, MSSA populations under selection from host and antibiotic accumulated mutations in the global regulator gene\n                  <jats:italic>codY<\/jats:italic>\n                  , which controls biofilm formation in\n                  <jats:italic>S. aureus.<\/jats:italic>\n                  These populations had indeed evolved more robust biofilms\u2014a trait linked to both virulence and antibiotic resistance\u2014suggesting evolution of one trait can confer multiple adaptive benefits. Mutations that arose in these genes were also enriched in clinical isolates associated with systemic infections in humans. Despite evolving in similar environments, MRSA and MSSA populations\u2014differing only in the presence of an intact accessory gene (\n                  <jats:italic>mecA)<\/jats:italic>\n                  \u2014proceeded on divergent evolutionary paths, with MSSA populations exhibiting more similarities across replicate populations. Our results underscore the importance of considering the host context as a critical driver of pathogen traits like virulence and antibiotic resistance.\n                <\/jats:p>","DOI":"10.1101\/2024.08.31.610628","type":"posted-content","created":{"date-parts":[[2024,9,1]],"date-time":"2024-09-01T03:05:10Z","timestamp":1725159910000},"source":"Crossref","is-referenced-by-count":1,"title":["Host and antibiotic jointly select for greater virulence in\n                  <i>Staphylococcus aureus<\/i>"],"prefix":"10.64898","author":[{"given":"Michelle","family":"Su","sequence":"first","affiliation":[{"name":"Emory University School of Medicine, Division of Infectious Diseases, Atlanta, Georgia, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5269-1630","authenticated-orcid":false,"given":"Kim L.","family":"Hoang","sequence":"additional","affiliation":[{"name":"Emory University School of Medicine, Division of Infectious Diseases, Atlanta, Georgia, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"McKenna","family":"Penley","sequence":"additional","affiliation":[{"name":"Department of Biology, Emory University, Atlanta, Georgia, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Michelle H.","family":"Davis","sequence":"additional","affiliation":[{"name":"Emory University School of Medicine, Division of Infectious Diseases, Atlanta, Georgia, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jennifer D.","family":"Gresham","sequence":"additional","affiliation":[{"name":"Department of Biology, Emory University, Atlanta, Georgia, USA"},{"name":"Science Department, Penn State Scranton, Dunmore, Pennsylvania, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Levi T.","family":"Morran","sequence":"additional","affiliation":[{"name":"Department of Biology, Emory University, Atlanta, Georgia, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Timothy D.","family":"Read","sequence":"additional","affiliation":[{"name":"Emory University School of Medicine, Division of Infectious Diseases, Atlanta, Georgia, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"54368","reference":[{"key":"2026021323350405000_2024.08.31.610628v4.1","doi-asserted-by":"publisher","DOI":"10.1128\/mbio.00346-24"},{"key":"2026021323350405000_2024.08.31.610628v4.2","doi-asserted-by":"publisher","DOI":"10.1038\/nrmicro3270"},{"key":"2026021323350405000_2024.08.31.610628v4.3","doi-asserted-by":"publisher","DOI":"10.1038\/s41396-020-0652-0"},{"key":"2026021323350405000_2024.08.31.610628v4.4","doi-asserted-by":"publisher","DOI":"10.1126\/sciadv.aax2950"},{"key":"2026021323350405000_2024.08.31.610628v4.5","doi-asserted-by":"crossref","unstructured":"Bae T , Banger AK , Wallace A , Glass EM , \u00c5slund F , Schneewind O , Missiakas DM . 2004. 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