ArticleCell host & microbe2013
Functional modularity of the arginine catabolic mobile element contributes to the success of USA300 methicillin-resistant Staphylococcus aureus.
Article in Cell host & microbe, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 132 papers.
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132 citing papers in PubMed, 206 citations in OpenAlex.
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- Epidemiologic and Clinical Divergence of MRSA USA100 and USA300 in the United States.Antibiotics (Basel, Switzerland) · 2026Article
- Reduced MGE burden, virulence optimization, and acid stress tolerance shape the clonal succession of MRSA ST59.Science advances · 2026Article
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- Molecular Mechanisms of Sepsis-Associated Acute Kidney Injury.Journal of the American Society of Nephrology : JASN · 2025Review
- Urease promotes pH homeostasis and growth ofJournal of bacteriology · 2025Article
- Evolution of polyamine resistance inmSphere · 2025Article
- Arginine at the host-pathogen interface.Infection and immunity · 2025Review
- Gradual loss of mobile genetic elements inISME communications · 2025Article
- Efficacy of pH-Responsive Surface Functionalized Titanium Screws in Treating Implant-associated S. aureus Osteomyelitis with Biofilms Formation.Advanced healthcare materials · 2025Article
- Restriction of arginine induces antibiotic tolerance in Staphylococcus aureus.Nature communications · 2024Article
- Salmonella Typhimurium exploits host polyamines for assembly of the type 3 secretion machinery.PLoS biology · 2024Article
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- Evolution of polyamine resistance inbioRxiv : the preprint server for biology · 2024Article
72 more citing papers are in PubMed but not listed here.
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7 authors at 1 institution in 1 country.
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Abstract
The USA300 community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA) lineage causes the majority of skin and soft tissue infections (SSTIs) and is highly associated with the carriage of the arginine catabolic mobile element (ACME). However, the contribution of ACME to USA300's success in SSTIs is not completely understood. We show that the constitutive ACME-encoded arginine-deiminase system (Arc) allows USA300 to thrive in acidic environments that mimic human skin. Consequently, the ACME-Arc system drives excessive production of host polyamines, compounds uniquely toxic to S. aureus. To mitigate this, ACME also encodes SpeG, a polyamine-resistance enzyme that is essential for combating excess host polyamines in a murine SSTI model. Inhibiting host polyamine production not only restored ΔspeG persistence within infected wounds but also severely altered the host healing process, implying that polyamines play an integral role in coordinating the wound-healing response. Together, these data underscore the functional modularity of ACME and its contribution to the success of USA300 CA-MRSA.
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