Regulation of the Staphylococcal Superantigen-Like Protein 1 Gene of Community-Associated Methicillin-Resistant <i>Staphylococcus aureus</i> in Murine Abscesses

• Main Authors: Daniel J. Bretl, Abdulaziz Elfessi, Hannah Watkins, William R. Schwan
• Format: Article
• Language: English
• Published: MDPI AG 2019-07-01
• Series: Toxins
• Subjects: mouse abscess; methicillin-resistant <i>Staphylococcus aureus</i>; lux fusion; superantigen-like protein; gene regulation; defined minimal medium
• Online Access: https://www.mdpi.com/2072-6651/11/7/391

Community-associated methicillin-resistant <i>Staphylococcus aureus</i> (CA-MRSA) causes substantial skin and soft tissue infections annually in the United States and expresses numerous virulence factors, including a family of toxins known as the staphylococcal superantigen-like (SSL) proteins. Many of the SSL protein structures have been determined and implicated in immune system avoidance, but the full scope that these proteins play in different infection contexts remains unknown and continues to warrant investigation. Analysis of <i>ssl</i> gene regulation may provide valuable information related to the function of these proteins. To determine the transcriptional regulation of the <i>ssl1</i> gene of CA-MRSA strain MW2, an <i>ssl1</i> promoter::lux fusion was constructed and transformed into <i>S.</i> <i>aureus</i> strains RN6390 and Newman. Resulting strains were grown in a defined minimal medium (DSM) broth and nutrient-rich brain-heart infusion (BHI) broth and expression was determined by luminescence. Transcription of <i>ssl1</i> was up-regulated and occurred earlier during growth in DSM broth compared to BHI broth suggesting expression is regulated by nutrient availability. RN6390 and Newman strains containing the <i>ssl1::lux</i> fusion were also used to analyze regulation in vivo using a mouse abscess model of infection. A marked increase in <i>ssl1</i> transcription occurred early during infection, suggesting <i>SSL1</i> is important during early stages of infection, perhaps to avoid the immune system.