Impact of the Regulators SigB, Rot, SarA and sarS on the Toxic Shock Tst Promoter and TSST-1 Expression in Staphylococcus aureus.
Identifieur interne : 000D32 ( Main/Exploration ); précédent : 000D31; suivant : 000D33Impact of the Regulators SigB, Rot, SarA and sarS on the Toxic Shock Tst Promoter and TSST-1 Expression in Staphylococcus aureus.
Auteurs : Diego O. Andrey [Suisse] ; Ambre Jousselin [Suisse] ; Maite Villanueva [Suisse] ; Adriana Renzoni [Suisse] ; Antoinette Monod [Suisse] ; Christine Barras [Suisse] ; Natalia Rodriguez [Suisse] ; William L. Kelley [Suisse]Source :
- PloS one [ 1932-6203 ] ; 2015.
Descripteurs français
- KwdFr :
- Entérotoxines (génétique), Entérotoxines (métabolisme), Facteur sigma (génétique), Facteur sigma (métabolisme), Ilots génomiques (génétique), Protéines bactériennes (génétique), Protéines bactériennes (métabolisme), Protéines de liaison à l'ADN (génétique), Protéines de liaison à l'ADN (métabolisme), Protéines de répression (génétique), Protéines de répression (métabolisme), Régions promotrices (génétique) (génétique), Régulation de l'expression des gènes bactériens (génétique), Staphylococcus aureus (métabolisme), Superantigènes (génétique), Superantigènes (métabolisme), Toxines bactériennes (génétique), Toxines bactériennes (métabolisme), Transactivateurs (génétique), Transactivateurs (métabolisme).
- MESH :
- génétique : Entérotoxines, Facteur sigma, Ilots génomiques, Protéines bactériennes, Protéines de liaison à l'ADN, Protéines de répression, Régions promotrices (génétique), Régulation de l'expression des gènes bactériens, Superantigènes, Toxines bactériennes, Transactivateurs.
- métabolisme : Entérotoxines, Facteur sigma, Protéines bactériennes, Protéines de liaison à l'ADN, Protéines de répression, Staphylococcus aureus, Superantigènes, Toxines bactériennes, Transactivateurs.
English descriptors
- KwdEn :
- Bacterial Proteins (genetics), Bacterial Proteins (metabolism), Bacterial Toxins (genetics), Bacterial Toxins (metabolism), DNA-Binding Proteins (genetics), DNA-Binding Proteins (metabolism), Enterotoxins (genetics), Enterotoxins (metabolism), Gene Expression Regulation, Bacterial (genetics), Genomic Islands (genetics), Promoter Regions, Genetic (genetics), Repressor Proteins (genetics), Repressor Proteins (metabolism), Sigma Factor (genetics), Sigma Factor (metabolism), Staphylococcus aureus (metabolism), Superantigens (genetics), Superantigens (metabolism), Trans-Activators (genetics), Trans-Activators (metabolism).
- MESH :
- chemical , genetics : Bacterial Proteins, Bacterial Toxins, DNA-Binding Proteins, Enterotoxins, Repressor Proteins, Sigma Factor, Superantigens, Trans-Activators.
- chemical , metabolism : Bacterial Proteins, Bacterial Toxins, DNA-Binding Proteins, Enterotoxins, Repressor Proteins, Sigma Factor, Superantigens, Trans-Activators.
- genetics : Gene Expression Regulation, Bacterial, Genomic Islands, Promoter Regions, Genetic.
- metabolism : Staphylococcus aureus.
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.
DOI: 10.1371/journal.pone.0135579
PubMed: 26275216
Affiliations:
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Le document en format XML
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Bacterial Proteins (genetics)</term>
<term>Bacterial Proteins (metabolism)</term>
<term>Bacterial Toxins (genetics)</term>
<term>Bacterial Toxins (metabolism)</term>
<term>DNA-Binding Proteins (genetics)</term>
<term>DNA-Binding Proteins (metabolism)</term>
<term>Enterotoxins (genetics)</term>
<term>Enterotoxins (metabolism)</term>
<term>Gene Expression Regulation, Bacterial (genetics)</term>
<term>Genomic Islands (genetics)</term>
<term>Promoter Regions, Genetic (genetics)</term>
<term>Repressor Proteins (genetics)</term>
<term>Repressor Proteins (metabolism)</term>
<term>Sigma Factor (genetics)</term>
<term>Sigma Factor (metabolism)</term>
<term>Staphylococcus aureus (metabolism)</term>
<term>Superantigens (genetics)</term>
<term>Superantigens (metabolism)</term>
<term>Trans-Activators (genetics)</term>
<term>Trans-Activators (metabolism)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Entérotoxines (génétique)</term>
<term>Entérotoxines (métabolisme)</term>
<term>Facteur sigma (génétique)</term>
<term>Facteur sigma (métabolisme)</term>
<term>Ilots génomiques (génétique)</term>
<term>Protéines bactériennes (génétique)</term>
<term>Protéines bactériennes (métabolisme)</term>
<term>Protéines de liaison à l'ADN (génétique)</term>
<term>Protéines de liaison à l'ADN (métabolisme)</term>
<term>Protéines de répression (génétique)</term>
<term>Protéines de répression (métabolisme)</term>
<term>Régions promotrices (génétique) (génétique)</term>
<term>Régulation de l'expression des gènes bactériens (génétique)</term>
<term>Staphylococcus aureus (métabolisme)</term>
<term>Superantigènes (génétique)</term>
<term>Superantigènes (métabolisme)</term>
<term>Toxines bactériennes (génétique)</term>
<term>Toxines bactériennes (métabolisme)</term>
<term>Transactivateurs (génétique)</term>
<term>Transactivateurs (métabolisme)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Bacterial Proteins</term>
<term>Bacterial Toxins</term>
<term>DNA-Binding Proteins</term>
<term>Enterotoxins</term>
<term>Repressor Proteins</term>
<term>Sigma Factor</term>
<term>Superantigens</term>
<term>Trans-Activators</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Bacterial Proteins</term>
<term>Bacterial Toxins</term>
<term>DNA-Binding Proteins</term>
<term>Enterotoxins</term>
<term>Repressor Proteins</term>
<term>Sigma Factor</term>
<term>Superantigens</term>
<term>Trans-Activators</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Gene Expression Regulation, Bacterial</term>
<term>Genomic Islands</term>
<term>Promoter Regions, Genetic</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Entérotoxines</term>
<term>Facteur sigma</term>
<term>Ilots génomiques</term>
<term>Protéines bactériennes</term>
<term>Protéines de liaison à l'ADN</term>
<term>Protéines de répression</term>
<term>Régions promotrices (génétique)</term>
<term>Régulation de l'expression des gènes bactériens</term>
<term>Superantigènes</term>
<term>Toxines bactériennes</term>
<term>Transactivateurs</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Staphylococcus aureus</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Entérotoxines</term>
<term>Facteur sigma</term>
<term>Protéines bactériennes</term>
<term>Protéines de liaison à l'ADN</term>
<term>Protéines de répression</term>
<term>Staphylococcus aureus</term>
<term>Superantigènes</term>
<term>Toxines bactériennes</term>
<term>Transactivateurs</term>
</keywords>
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<front><div type="abstract" xml:lang="en">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. </div>
</front>
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<tree><country name="Suisse"><noRegion><name sortKey="Andrey, Diego O" sort="Andrey, Diego O" uniqKey="Andrey D" first="Diego O" last="Andrey">Diego O. Andrey</name>
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<name sortKey="Barras, Christine" sort="Barras, Christine" uniqKey="Barras C" first="Christine" last="Barras">Christine Barras</name>
<name sortKey="Jousselin, Ambre" sort="Jousselin, Ambre" uniqKey="Jousselin A" first="Ambre" last="Jousselin">Ambre Jousselin</name>
<name sortKey="Kelley, William L" sort="Kelley, William L" uniqKey="Kelley W" first="William L" last="Kelley">William L. Kelley</name>
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<name sortKey="Renzoni, Adriana" sort="Renzoni, Adriana" uniqKey="Renzoni A" first="Adriana" last="Renzoni">Adriana Renzoni</name>
<name sortKey="Rodriguez, Natalia" sort="Rodriguez, Natalia" uniqKey="Rodriguez N" first="Natalia" last="Rodriguez">Natalia Rodriguez</name>
<name sortKey="Villanueva, Maite" sort="Villanueva, Maite" uniqKey="Villanueva M" first="Maite" last="Villanueva">Maite Villanueva</name>
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