Prophage-encoded methyltransferase drives adaptation of community-acquired methicillin-resistant Staphylococcus aureus.

Robert J Ulrich,Magdalena Podkowik, Rebecca Tierce,Irnov Irnov,Gregory Putzel, Nora Samhadaneh,Keenan A Lacey, Daiane Boff, Sabrina M Morales, Sohei Makita, Theodora K Karagounis,Erin E Zwack,Chunyi Zhou, Randie Kim,Karl Drlica,Alejandro Pironti,Harm van Bakel,Victor J Torres,Bo Shopsin

bioRxiv : the preprint server for biology(2024)

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摘要
We recently described the evolution of a community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA) USA300 variant responsible for an outbreak of skin and soft tissue infections. Acquisition of a mosaic version of the Φ11 prophage (mΦ11) 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 mΦ11 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 mΦ11-encoded adenine methyltransferase (designated pamA ). pamA increased expression of fibronectin-binding protein A ( fnbA ; FnBPA), and inactivation of fnbA eliminated the effect of pamA on abscess virulence without affecting strains lacking pamA . Thus, fnbA is a pamA -specific virulence factor. Mechanistically, pamA was shown to promote biofilm formation in vivo in skin abscesses, a phenotype linked to FnBPA's role in biofilm formation. Collectively, these data reveal a novel mechanism-epigenetic regulation of staphylococcal gene expression-by which phage can regulate virulence to drive adaptive leaps by S. aureus .
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