ArticlePloS one2015
Impact of the Regulators SigB, Rot, SarA and sarS on the Toxic Shock Tst Promoter and TSST-1 Expression in Staphylococcus aureus.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 44 citations in OpenAlex.
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- Toxic Shock Syndrome Toxin-1 (TSST-1) inToxins · 2025Review
- In Silico Hybridization and Molecular Dynamics Simulations for the Identification of Candidate Human MicroRNAs for Inhibition of Virulent Proteins' Expression in Staphylococcus aureus.Journal of cellular biochemistry · 2025Article
- Surface Topography, Microbial Adhesion, and Immune Responses in Silicone Mammary Implant-Associated Capsular Fibrosis.International journal of molecular sciences · 2024Article
- Coordination of prophage and global regulator leads to high enterotoxin production in staphylococcal food poisoning-associated lineage.Microbiology spectrum · 2024Article
- Horizontal transfer of probable chicken-pathogenicity chromosomal islands between Staphylococcus aureus and Staphylococcus agnetis.PloS one · 2023Article
- PurN Is Involved in Antibiotic Tolerance and Virulence inAntibiotics (Basel, Switzerland) · 2022Article
- Superantigens, a Paradox of the Immune Response.Toxins · 2022Review
- Sterilization Procedures for Titanium Alloy Surfaces Leads to Higher Expression of Biofilm-RelatedAntibiotics (Basel, Switzerland) · 2022Article
- Glucose Mediates Niche-Specific Repression of Staphylococcus aureus Toxic Shock Syndrome Toxin-1 through the Activity of CcpA in the Vaginal Environment.Journal of bacteriology · 2022Article
- Antibiofilm Activity of Omega-3 Fatty Acids and Its Influence on the Expression of Biofilm Formation Genes onAntibiotics (Basel, Switzerland) · 2022Article
- The Association Between Onset of Staphylococcal Non-menstrual Toxic Shock Syndrome With Inducibility of Toxic Shock Syndrome Toxin-1 Production.Frontiers in microbiology · 2022Article
- Vegetation Formation inFrontiers in cellular and infection microbiology · 2022Article
- Host factors abolish the need for polysaccharides and extracellular matrix-binding protein inJournal of medical microbiology · 2021Article
- Molecular Mechanisms ofFrontiers in cellular and infection microbiology · 2021Review
- Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Staphylococcus aureus is an important pathogen manifesting virulence through diverse disease forms, ranging from acute skin infections to life-threatening bacteremia or systemic toxic shock syndromes. In the latter case, the prototypical superantigen is TSST-1 (Toxic Shock Syndrome Toxin 1), encoded by tst(H), and carried on a mobile genetic element that is not present in all S. aureus strains. Transcriptional regulation of tst is only partially understood. In this study, we dissected the role of sarA, sarS (sarH1), RNAIII, rot, and the alternative stress sigma factor sigB (σB). By examining tst promoter regulation predominantly in the context of its native sequence within the SaPI1 pathogenicity island of strain RN4282, we discovered that σB emerged as a particularly important tst regulator. We did not detect a consensus σB site within the tst promoter, and thus the effect of σB is likely indirect. We found that σB strongly repressed the expression of the toxin via at least two distinct regulatory pathways dependent upon sarA and agr. Furthermore rot, a member of SarA family, was shown to repress tst expression when overexpressed, although its deletion had no consistent measurable effect. We could not find any detectable effect of sarS, either by deletion or overexpression, suggesting that this regulator plays a minimal role in TSST-1 expression except when combined with disruption of sarA. Collectively, our results extend our understanding of complex multifactorial regulation of tst, revealing several layers of negative regulation. In addition to environmental stimuli thought to impact TSST-1 production, these findings support a model whereby sporadic mutation in a few key negative regulators can profoundly affect and enhance TSST-1 expression.
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