DetoxFungiV1, Main, Exploration, bibRecord, 001043

Control of Clostridium difficile Physiopathology in Response to Cysteine Availability.

Identifieur interne : 001043 ( Main/Exploration ); précédent : 001042; suivant : 001044

Control of Clostridium difficile Physiopathology in Response to Cysteine Availability.

Auteurs : Thomas Dubois [France] ; Marie Dancer-Thibonnier [France] ; Marc Monot [France] ; Audrey Hamiot [France] ; Laurent Bouillaut [États-Unis] ; Olga Soutourina [France] ; Isabelle Martin-Verstraete [France] ; Bruno Dupuy [France]

Source :

Infection and immunity [ 1098-5522 ] ; 2016.

RBID : pubmed:27297391

Descripteurs français

KwdFr :
- Acide pyruvique (métabolisme), Acides aminés (métabolisme), Animaux (MeSH), Cellules Vero (MeSH), Clostridium difficile (physiologie), Cystéine (métabolisme), Entérocolite pseudomembraneuse (microbiologie), Espace intracellulaire (métabolisme), Homocystéine (métabolisme), Lignée cellulaire (MeSH), Métabolisme énergétique (génétique), Régulation de l'expression des gènes bactériens (MeSH), Sulfure d'hydrogène (métabolisme), Toxines bactériennes (biosynthèse), Toxines bactériennes (génétique), Voies et réseaux métaboliques (MeSH).
MESH :
- biosynthèse : Toxines bactériennes.
- génétique : Métabolisme énergétique, Toxines bactériennes.
- microbiologie : Entérocolite pseudomembraneuse.
- métabolisme : Acide pyruvique, Acides aminés, Cystéine, Espace intracellulaire, Homocystéine, Sulfure d'hydrogène.
- physiologie : Clostridium difficile.
- Animaux, Cellules Vero, Lignée cellulaire, Régulation de l'expression des gènes bactériens, Voies et réseaux métaboliques.

English descriptors

KwdEn :
- Amino Acids (metabolism), Animals (MeSH), Bacterial Toxins (biosynthesis), Bacterial Toxins (genetics), Cell Line (MeSH), Chlorocebus aethiops (MeSH), Clostridium difficile (physiology), Cysteine (metabolism), Energy Metabolism (genetics), Enterocolitis, Pseudomembranous (microbiology), Gene Expression Regulation, Bacterial (MeSH), Homocysteine (metabolism), Hydrogen Sulfide (metabolism), Intracellular Space (metabolism), Metabolic Networks and Pathways (MeSH), Pyruvic Acid (metabolism), Vero Cells (MeSH).
MESH :
- chemical , biosynthesis : Bacterial Toxins.
- chemical , genetics : Bacterial Toxins.
- chemical , metabolism : Amino Acids, Cysteine, Homocysteine, Hydrogen Sulfide, Pyruvic Acid.
- genetics : Energy Metabolism.
- metabolism : Intracellular Space.
- microbiology : Enterocolitis, Pseudomembranous.
- physiology : Clostridium difficile.
- Animals, Cell Line, Chlorocebus aethiops, Gene Expression Regulation, Bacterial, Metabolic Networks and Pathways, Vero Cells.

Abstract

The pathogenicity of Clostridium difficile is linked to its ability to produce two toxins: TcdA and TcdB. The level of toxin synthesis is influenced by environmental signals, such as phosphotransferase system (PTS) sugars, biotin, and amino acids, especially cysteine. To understand the molecular mechanisms of cysteine-dependent repression of toxin production, we reconstructed the sulfur metabolism pathways of C. difficile strain 630 in silico and validated some of them by testing C. difficile growth in the presence of various sulfur sources. High levels of sulfide and pyruvate were produced in the presence of 10 mM cysteine, indicating that cysteine is actively catabolized by cysteine desulfhydrases. Using a transcriptomic approach, we analyzed cysteine-dependent control of gene expression and showed that cysteine modulates the expression of genes involved in cysteine metabolism, amino acid biosynthesis, fermentation, energy metabolism, iron acquisition, and the stress response. Additionally, a sigma factor (SigL) and global regulators (CcpA, CodY, and Fur) were tested to elucidate their roles in the cysteine-dependent regulation of toxin production. Among these regulators, only sigL inactivation resulted in the derepression of toxin gene expression in the presence of cysteine. Interestingly, the sigL mutant produced less pyruvate and H2S than the wild-type strain. Unlike cysteine, the addition of 10 mM pyruvate to the medium for a short time during the growth of the wild-type and sigL mutant strains reduced expression of the toxin genes, indicating that cysteine-dependent repression of toxin production is mainly due to the accumulation of cysteine by-products during growth. Finally, we showed that the effect of pyruvate on toxin gene expression is mediated at least in part by the two-component system CD2602-CD2601.

DOI: 10.1128/IAI.00121-16
PubMed: 27297391
PubMed Central: PMC4962627

Affiliations:

Links toward previous steps (curation, corpus...)

to stream Main, to step Corpus: 000E99
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Le document en format XML

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<term>Animals (MeSH)</term>
<term>Bacterial Toxins (biosynthesis)</term>
<term>Bacterial Toxins (genetics)</term>
<term>Cell Line (MeSH)</term>
<term>Chlorocebus aethiops (MeSH)</term>
<term>Clostridium difficile (physiology)</term>
<term>Cysteine (metabolism)</term>
<term>Energy Metabolism (genetics)</term>
<term>Enterocolitis, Pseudomembranous (microbiology)</term>
<term>Gene Expression Regulation, Bacterial (MeSH)</term>
<term>Homocysteine (metabolism)</term>
<term>Hydrogen Sulfide (metabolism)</term>
<term>Intracellular Space (metabolism)</term>
<term>Metabolic Networks and Pathways (MeSH)</term>
<term>Pyruvic Acid (metabolism)</term>
<term>Vero Cells (MeSH)</term>
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<keywords scheme="KwdFr" xml:lang="fr"><term>Acide pyruvique (métabolisme)</term>
<term>Acides aminés (métabolisme)</term>
<term>Animaux (MeSH)</term>
<term>Cellules Vero (MeSH)</term>
<term>Clostridium difficile (physiologie)</term>
<term>Cystéine (métabolisme)</term>
<term>Entérocolite pseudomembraneuse (microbiologie)</term>
<term>Espace intracellulaire (métabolisme)</term>
<term>Homocystéine (métabolisme)</term>
<term>Lignée cellulaire (MeSH)</term>
<term>Métabolisme énergétique (génétique)</term>
<term>Régulation de l'expression des gènes bactériens (MeSH)</term>
<term>Sulfure d'hydrogène (métabolisme)</term>
<term>Toxines bactériennes (biosynthèse)</term>
<term>Toxines bactériennes (génétique)</term>
<term>Voies et réseaux métaboliques (MeSH)</term>
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<keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Bacterial Toxins</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Bacterial Toxins</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Amino Acids</term>
<term>Cysteine</term>
<term>Homocysteine</term>
<term>Hydrogen Sulfide</term>
<term>Pyruvic Acid</term>
</keywords>
<keywords scheme="MESH" qualifier="biosynthèse" xml:lang="fr"><term>Toxines bactériennes</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Energy Metabolism</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Métabolisme énergétique</term>
<term>Toxines bactériennes</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Intracellular Space</term>
</keywords>
<keywords scheme="MESH" qualifier="microbiologie" xml:lang="fr"><term>Entérocolite pseudomembraneuse</term>
</keywords>
<keywords scheme="MESH" qualifier="microbiology" xml:lang="en"><term>Enterocolitis, Pseudomembranous</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Acide pyruvique</term>
<term>Acides aminés</term>
<term>Cystéine</term>
<term>Espace intracellulaire</term>
<term>Homocystéine</term>
<term>Sulfure d'hydrogène</term>
</keywords>
<keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Clostridium difficile</term>
</keywords>
<keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Clostridium difficile</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Cell Line</term>
<term>Chlorocebus aethiops</term>
<term>Gene Expression Regulation, Bacterial</term>
<term>Metabolic Networks and Pathways</term>
<term>Vero Cells</term>
</keywords>
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<term>Cellules Vero</term>
<term>Lignée cellulaire</term>
<term>Régulation de l'expression des gènes bactériens</term>
<term>Voies et réseaux métaboliques</term>
</keywords>
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<front><div type="abstract" xml:lang="en">The pathogenicity of Clostridium difficile is linked to its ability to produce two toxins: TcdA and TcdB. The level of toxin synthesis is influenced by environmental signals, such as phosphotransferase system (PTS) sugars, biotin, and amino acids, especially cysteine. To understand the molecular mechanisms of cysteine-dependent repression of toxin production, we reconstructed the sulfur metabolism pathways of C. difficile strain 630 in silico and validated some of them by testing C. difficile growth in the presence of various sulfur sources. High levels of sulfide and pyruvate were produced in the presence of 10 mM cysteine, indicating that cysteine is actively catabolized by cysteine desulfhydrases. Using a transcriptomic approach, we analyzed cysteine-dependent control of gene expression and showed that cysteine modulates the expression of genes involved in cysteine metabolism, amino acid biosynthesis, fermentation, energy metabolism, iron acquisition, and the stress response. Additionally, a sigma factor (SigL) and global regulators (CcpA, CodY, and Fur) were tested to elucidate their roles in the cysteine-dependent regulation of toxin production. Among these regulators, only sigL inactivation resulted in the derepression of toxin gene expression in the presence of cysteine. Interestingly, the sigL mutant produced less pyruvate and H2S than the wild-type strain. Unlike cysteine, the addition of 10 mM pyruvate to the medium for a short time during the growth of the wild-type and sigL mutant strains reduced expression of the toxin genes, indicating that cysteine-dependent repression of toxin production is mainly due to the accumulation of cysteine by-products during growth. Finally, we showed that the effect of pyruvate on toxin gene expression is mediated at least in part by the two-component system CD2602-CD2601.</div>
</front>
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<Month>05</Month>
<Day>16</Day>
</DateCompleted>
<DateRevised><Year>2019</Year>
<Month>12</Month>
<Day>10</Day>
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<Month>08</Month>
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<ISOAbbreviation>Infect Immun</ISOAbbreviation>
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<ArticleTitle>Control of Clostridium difficile Physiopathology in Response to Cysteine Availability.</ArticleTitle>
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<Abstract><AbstractText>The pathogenicity of Clostridium difficile is linked to its ability to produce two toxins: TcdA and TcdB. The level of toxin synthesis is influenced by environmental signals, such as phosphotransferase system (PTS) sugars, biotin, and amino acids, especially cysteine. To understand the molecular mechanisms of cysteine-dependent repression of toxin production, we reconstructed the sulfur metabolism pathways of C. difficile strain 630 in silico and validated some of them by testing C. difficile growth in the presence of various sulfur sources. High levels of sulfide and pyruvate were produced in the presence of 10 mM cysteine, indicating that cysteine is actively catabolized by cysteine desulfhydrases. Using a transcriptomic approach, we analyzed cysteine-dependent control of gene expression and showed that cysteine modulates the expression of genes involved in cysteine metabolism, amino acid biosynthesis, fermentation, energy metabolism, iron acquisition, and the stress response. Additionally, a sigma factor (SigL) and global regulators (CcpA, CodY, and Fur) were tested to elucidate their roles in the cysteine-dependent regulation of toxin production. Among these regulators, only sigL inactivation resulted in the derepression of toxin gene expression in the presence of cysteine. Interestingly, the sigL mutant produced less pyruvate and H2S than the wild-type strain. Unlike cysteine, the addition of 10 mM pyruvate to the medium for a short time during the growth of the wild-type and sigL mutant strains reduced expression of the toxin genes, indicating that cysteine-dependent repression of toxin production is mainly due to the accumulation of cysteine by-products during growth. Finally, we showed that the effect of pyruvate on toxin gene expression is mediated at least in part by the two-component system CD2602-CD2601.</AbstractText>
<CopyrightInformation>Copyright © 2016, American Society for Microbiology. All Rights Reserved.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Dubois</LastName>
<ForeName>Thomas</ForeName>
<Initials>T</Initials>
<AffiliationInfo><Affiliation>Laboratoire Pathogenèse des Bactéries Anaérobies, Institut Pasteur, Paris, France.</Affiliation>
</AffiliationInfo>
</Author>
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<name sortKey="Soutourina, Olga" sort="Soutourina, Olga" uniqKey="Soutourina O" first="Olga" last="Soutourina">Olga Soutourina</name>
</country>
<country name="États-Unis"><region name="Massachusetts"><name sortKey="Bouillaut, Laurent" sort="Bouillaut, Laurent" uniqKey="Bouillaut L" first="Laurent" last="Bouillaut">Laurent Bouillaut</name>
</region>
</country>
</tree>
</affiliations>
</record>

Pour manipuler ce document sous Unix (Dilib)

EXPLOR_STEP=$WICRI_ROOT/Bois/explor/DetoxFungiV1/Data/Main/Exploration

HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 001043 | SxmlIndent | more

HfdSelect -h $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd -nk 001043 | SxmlIndent | more

Pour mettre un lien sur cette page dans le réseau Wicri

{{Explor lien
   |wiki=    Bois
   |area=    DetoxFungiV1
   |flux=    Main
   |étape=   Exploration
   |type=    RBID
   |clé=     pubmed:27297391
   |texte=   Control of Clostridium difficile Physiopathology in Response to Cysteine Availability.
}}

Pour générer des pages wiki

HfdIndexSelect -h $EXPLOR_AREA/Data/Main/Exploration/RBID.i   -Sk "pubmed:27297391" \
       | HfdSelect -Kh $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd   \
       | NlmPubMed2Wicri -a DetoxFungiV1

This area was generated with Dilib version V0.6.38.
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	Serveur d'exploration sur la détoxication des champignons
	Attention, ce site est en cours de développement ! Attention, site généré par des moyens informatiques à partir de corpus bruts. Les informations ne sont donc pas validées.

Serveur d'exploration sur la détoxication des champignons

Control of Clostridium difficile Physiopathology in Response to Cysteine Availability.

Control of Clostridium difficile Physiopathology in Response to Cysteine Availability.

Source :

Descripteurs français

English descriptors

Abstract

Links toward previous steps (curation, corpus...)

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri

Pour générer des pages wiki