A Functional ClpXP Protease is Required for Induction of the Accessory Toxin Genes, tst, sed, and sec
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A Functional ClpXP Protease is Required for Induction of the Accessory Toxin Genes, tst, sed, and sec. / Schelin, Jenny; Cohn, Marianne Thorup; Frisk, Barbro; Frees, Dorte.
I: Toxins, Bind 12, Nr. 9, 553, 2020.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt
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T1 - A Functional ClpXP Protease is Required for Induction of the Accessory Toxin Genes, tst, sed, and sec
AU - Schelin, Jenny
AU - Cohn, Marianne Thorup
AU - Frisk, Barbro
AU - Frees, Dorte
PY - 2020
Y1 - 2020
N2 - 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.
AB - 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.
KW - ClpXP
KW - Mobile genetic elements
KW - RNA‐seq
KW - Staphylococcal enterotoxins
KW - Staphylococcus aureus
KW - TSST‐1
KW - Virulence gene regulation
U2 - 10.3390/toxins12090553
DO - 10.3390/toxins12090553
M3 - Journal article
C2 - 32872362
AN - SCOPUS:85090180478
VL - 12
JO - Toxins
JF - Toxins
SN - 2072-6651
IS - 9
M1 - 553
ER -
ID: 248460818