{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"institution":[{"name":"bioRxiv"}],"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T01:05:34Z","timestamp":1790730334468,"version":"4.1.0"},"posted":{"date-parts":[[2024,4,17]]},"group-title":"Microbiology","reference-count":79,"publisher":"openRxiv","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"accepted":{"date-parts":[[2024,4,17]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                <jats:p>\n                  We recently described the evolution of a community-acquired methicillin-resistant\n                  <jats:italic>Staphylococcus aureus<\/jats:italic>\n                  (CA-MRSA) USA300 variant responsible for an outbreak of skin and soft tissue infections. Acquisition of a mosaic version of the \u03a611 prophage (m\u03a611) that increases skin abscess size was an early step in CA-MRSA adaptation that primed the successful spread of the clone. The present report shows how prophage m\u03a611 exerts its effect on virulence for skin infection without encoding a known toxin or fitness genes. Abscess size and skin inflammation were associated with DNA methylase activity of an m\u03a611-encoded adenine methyltransferase (designated\n                  <jats:italic>pamA<\/jats:italic>\n                  ).\n                  <jats:italic>pamA<\/jats:italic>\n                  increased expression of fibronectin-binding protein A (\n                  <jats:italic>fnbA<\/jats:italic>\n                  ; FnBPA), and inactivation of\n                  <jats:italic>fnbA<\/jats:italic>\n                  eliminated the effect of\n                  <jats:italic>pamA<\/jats:italic>\n                  on abscess virulence without affecting strains lacking\n                  <jats:italic>pamA<\/jats:italic>\n                  . Thus,\n                  <jats:italic>fnbA<\/jats:italic>\n                  is a\n                  <jats:italic>pamA<\/jats:italic>\n                  -specific virulence factor. Mechanistically,\n                  <jats:italic>pamA<\/jats:italic>\n                  was shown to promote biofilm formation in vivo in skin abscesses, a phenotype linked to FnBPA\u2019s role in biofilm formation. Collectively, these data reveal a novel mechanism\u2014epigenetic regulation of staphylococcal gene expression\u2014by which phage can regulate virulence to drive adaptive leaps by\n                  <jats:italic>S. aureus<\/jats:italic>\n                  .\n                <\/jats:p>\n                <jats:sec>\n                  <jats:title>Graphical Abstract<\/jats:title>\n                  <jats:fig id=\"ufig1\" position=\"float\" orientation=\"portrait\" fig-type=\"figure\">\n                    <jats:graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"589803v1_ufig1\" position=\"float\" orientation=\"portrait\"\/>\n                  <\/jats:fig>\n                <\/jats:sec>","DOI":"10.1101\/2024.04.17.589803","type":"posted-content","created":{"date-parts":[[2024,4,18]],"date-time":"2024-04-18T00:40:10Z","timestamp":1713400810000},"source":"Crossref","is-referenced-by-count":4,"title":["Prophage-encoded methyltransferase drives adaptation of community-acquired methicillin-resistant\n                  <i>Staphylococcus aureus<\/i>"],"prefix":"10.64898","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-3217-5062","authenticated-orcid":false,"given":"Robert 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