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Abstract
Staphylococcal toxic shock syndrome is a potentially lethal illness attributed to superantigens produced by Staphylococcus aureus, in particular toxic shock syndrome toxin 1 (TSST-1), but staphylococcal enterotoxins (SEs) are also implicated. The genes encoding these important toxins are carried on mobile genetic elements, and the regulatory networks controlling expression of these toxins remain relatively unexplored. We show here that the highly conserved ClpXP protease stimulates transcription of tst (TSST-1), sec (SEC), and sed (SED) genes in the prototypical strains, SA564 and RN4282. In the wild-type cells, the post-exponential upregulation of toxin gene transcription was proposed to occur via RNAIII-mediated downregulation of the Rot repressor. Contradictive to this model, we showed that the post-exponential induction of tst, sed, and sec transcription did not occur in cells devoid of ClpXP activity, despite the Rot level being diminished. To identify transcriptional regulators with a changed expression in cells devoid of ClpXP activity, RNA sequencing was performed. The RNAseq analysis revealed a number of global virulence regulators that might act downstream of ClpXP, to control expression of tst and other virulence genes. Collectively, the results extend our understanding of the complex transcriptional regulation of the tst, sed, and sec genes.
Highlights
Staphylococcus aureus colonizes the anterior nares and the skin of approximately 30% of the human population
To examine the role of ClpXP in transcriptional regulation of toxin genes encoded by mobile genetic elements we chose strain SA564, a CC5/t648 strain recovered from a patient with toxic shock syndrome, as a model [31]
In SA564, the tst gene is encoded by a S. aureus pathogenicity island that is closely related to SaPIn1 in strain N315 and which carries the sec gene [32,33]
Summary
Staphylococcus aureus colonizes the anterior nares and the skin of approximately 30% of the human population. While most S. aureus infections involve the coordinated expression of numerous virulence factors, a few select diseases, including TSS, are mediated by single staphylococcal exotoxins, belonging to the family of S. aureus superantigens (SAgs) [2,3]. These SAg exotoxins lead to massive activation of T cells, and symptoms associated with TSS include, fever, skin rash, desquamation, hypotension, and hemodynamic shock [4,5]. Toxins 2020, 12, 553 the toxic shock syndrome toxin 1 (TSST-1) [3] This toxin is the causative agent of approximately half of all surgical-related TSS cases [3].
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