BiopestPeptidV1, Main, Exploration, bibRecord, 000914

Epistatic control of intrinsic resistance by virulence genes in Listeria.

Identifieur interne : 000914 ( Main/Exploration ); précédent : 000913; suivant : 000915

Epistatic control of intrinsic resistance by virulence genes in Listeria.

Auteurs : Mariela Scortti [Royaume-Uni] ; Lei Han [Royaume-Uni] ; Sonsiray Alvarez [Royaume-Uni] ; Alexandre Leclercq [France] ; Alexandra Moura [France] ; Marc Lecuit [France] ; Jose Vazquez-Boland [Royaume-Uni]

Source :

PLoS genetics [ 1553-7404 ] ; 2018.

RBID : pubmed:30180166

Descripteurs français

KwdFr :
- Antibactériens (pharmacologie), Antibactériens (usage thérapeutique), Facteurs terminaison chaîne peptidique (génétique), Facteurs terminaison chaîne peptidique (métabolisme), Fosfomycine (pharmacologie), Fosfomycine (usage thérapeutique), Glutathione transferase (génétique), Glutathione transferase (métabolisme), Infections à Listeria (microbiologie), Infections à Listeria (traitement médicamenteux), Listeria monocytogenes (effets des médicaments et des substances chimiques), Listeria monocytogenes (pathogénicité), Listeria monocytogenes (physiologie), Protéines bactériennes (génétique), Protéines bactériennes (métabolisme), Protéines de transport membranaire (génétique), Protéines de transport membranaire (métabolisme), Régulation de l'expression des gènes bactériens (effets des médicaments et des substances chimiques), Régulation de l'expression des gènes bactériens (physiologie), Régulon (physiologie), Résistance bactérienne aux médicaments (effets des médicaments et des substances chimiques), Résistance bactérienne aux médicaments (génétique), Virulence (génétique), Épistasie (physiologie).
MESH :
- effets des médicaments et des substances chimiques : Listeria monocytogenes, Régulation de l'expression des gènes bactériens, Résistance bactérienne aux médicaments.
- génétique : Facteurs terminaison chaîne peptidique, Glutathione transferase, Protéines bactériennes, Protéines de transport membranaire, Résistance bactérienne aux médicaments, Virulence.
- microbiologie : Infections à Listeria.
- métabolisme : Facteurs terminaison chaîne peptidique, Glutathione transferase, Protéines bactériennes, Protéines de transport membranaire.
- pathogénicité : Listeria monocytogenes.
- pharmacologie : Antibactériens, Fosfomycine.
- physiologie : Listeria monocytogenes, Régulation de l'expression des gènes bactériens, Régulon, Épistasie.
- traitement médicamenteux : Infections à Listeria.
- usage thérapeutique : Antibactériens, Fosfomycine.

English descriptors

KwdEn :
- Anti-Bacterial Agents (pharmacology), Anti-Bacterial Agents (therapeutic use), Bacterial Proteins (genetics), Bacterial Proteins (metabolism), Drug Resistance, Bacterial (drug effects), Drug Resistance, Bacterial (genetics), Epistasis, Genetic (physiology), Fosfomycin (pharmacology), Fosfomycin (therapeutic use), Gene Expression Regulation, Bacterial (drug effects), Gene Expression Regulation, Bacterial (physiology), Glutathione Transferase (genetics), Glutathione Transferase (metabolism), Listeria monocytogenes (drug effects), Listeria monocytogenes (pathogenicity), Listeria monocytogenes (physiology), Listeriosis (drug therapy), Listeriosis (microbiology), Membrane Transport Proteins (genetics), Membrane Transport Proteins (metabolism), Peptide Termination Factors (genetics), Peptide Termination Factors (metabolism), Regulon (physiology), Virulence (genetics).
MESH :
- chemical , genetics : Bacterial Proteins, Glutathione Transferase, Membrane Transport Proteins, Peptide Termination Factors.
- chemical , metabolism : Bacterial Proteins, Glutathione Transferase, Membrane Transport Proteins, Peptide Termination Factors.
- chemical , pharmacology : Anti-Bacterial Agents, Fosfomycin.
- chemical , therapeutic use : Anti-Bacterial Agents, Fosfomycin.
- drug effects : Drug Resistance, Bacterial, Gene Expression Regulation, Bacterial, Listeria monocytogenes.
- drug therapy : Listeriosis.
- genetics : Drug Resistance, Bacterial, Virulence.
- microbiology : Listeriosis.
- pathogenicity : Listeria monocytogenes.
- physiology : Epistasis, Genetic, Gene Expression Regulation, Bacterial, Listeria monocytogenes, Regulon.

Abstract

Elucidating the relationships between antimicrobial resistance and virulence is key to understanding the evolution and population dynamics of resistant pathogens. Here, we show that the susceptibility of the gram-positive bacterium Listeria monocytogenes to the antibiotic fosfomycin is a complex trait involving interactions between resistance and virulence genes and the environment. We found that a FosX enzyme encoded in the listerial core genome confers intrinsic fosfomycin resistance to both pathogenic and non-pathogenic Listeria spp. However, in the genomic context of the pathogenic L. monocytogenes, FosX-mediated resistance is epistatically suppressed by two members of the PrfA virulence regulon, hpt and prfA, which upon activation by host signals induce increased fosfomycin influx into the bacterial cell. Consequently, in infection conditions, most L. monocytogenes isolates become susceptible to fosfomycin despite possessing a gene that confers high-level resistance to the drug. Our study establishes the molecular basis of an epistatic interaction between virulence and resistance genes controlling bacterial susceptibility to an antibiotic. The reported findings provide the rationale for the introduction of fosfomycin in the treatment of Listeria infections even though these bacteria are intrinsically resistant to the antibiotic in vitro.

DOI: 10.1371/journal.pgen.1007525
PubMed: 30180166
PubMed Central: PMC6122793

Affiliations:

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

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to stream Main, to step Curation: 000694

Le document en format XML

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<term>Protéines de transport membranaire</term>
<term>Résistance bactérienne aux médicaments</term>
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<keywords scheme="MESH" qualifier="microbiology" xml:lang="en"><term>Listeriosis</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Facteurs terminaison chaîne peptidique</term>
<term>Glutathione transferase</term>
<term>Protéines bactériennes</term>
<term>Protéines de transport membranaire</term>
</keywords>
<keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>Listeria monocytogenes</term>
</keywords>
<keywords scheme="MESH" qualifier="pathogénicité" xml:lang="fr"><term>Listeria monocytogenes</term>
</keywords>
<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Antibactériens</term>
<term>Fosfomycine</term>
</keywords>
<keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Listeria monocytogenes</term>
<term>Régulation de l'expression des gènes bactériens</term>
<term>Régulon</term>
<term>Épistasie</term>
</keywords>
<keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Epistasis, Genetic</term>
<term>Gene Expression Regulation, Bacterial</term>
<term>Listeria monocytogenes</term>
<term>Regulon</term>
</keywords>
<keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Infections à Listeria</term>
</keywords>
<keywords scheme="MESH" qualifier="usage thérapeutique" xml:lang="fr"><term>Antibactériens</term>
<term>Fosfomycine</term>
</keywords>
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<front><div type="abstract" xml:lang="en">Elucidating the relationships between antimicrobial resistance and virulence is key to understanding the evolution and population dynamics of resistant pathogens. Here, we show that the susceptibility of the gram-positive bacterium Listeria monocytogenes to the antibiotic fosfomycin is a complex trait involving interactions between resistance and virulence genes and the environment. We found that a FosX enzyme encoded in the listerial core genome confers intrinsic fosfomycin resistance to both pathogenic and non-pathogenic Listeria spp. However, in the genomic context of the pathogenic L. monocytogenes, FosX-mediated resistance is epistatically suppressed by two members of the PrfA virulence regulon, hpt and prfA, which upon activation by host signals induce increased fosfomycin influx into the bacterial cell. Consequently, in infection conditions, most L. monocytogenes isolates become susceptible to fosfomycin despite possessing a gene that confers high-level resistance to the drug. Our study establishes the molecular basis of an epistatic interaction between virulence and resistance genes controlling bacterial susceptibility to an antibiotic. The reported findings provide the rationale for the introduction of fosfomycin in the treatment of Listeria infections even though these bacteria are intrinsically resistant to the antibiotic in vitro.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">30180166</PMID>
<DateCompleted><Year>2019</Year>
<Month>01</Month>
<Day>15</Day>
</DateCompleted>
<DateRevised><Year>2019</Year>
<Month>01</Month>
<Day>15</Day>
</DateRevised>
<Article PubModel="Electronic-eCollection"><Journal><ISSN IssnType="Electronic">1553-7404</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>14</Volume>
<Issue>9</Issue>
<PubDate><Year>2018</Year>
<Month>09</Month>
</PubDate>
</JournalIssue>
<Title>PLoS genetics</Title>
<ISOAbbreviation>PLoS Genet</ISOAbbreviation>
</Journal>
<ArticleTitle>Epistatic control of intrinsic resistance by virulence genes in Listeria.</ArticleTitle>
<Pagination><MedlinePgn>e1007525</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1371/journal.pgen.1007525</ELocationID>
<Abstract><AbstractText>Elucidating the relationships between antimicrobial resistance and virulence is key to understanding the evolution and population dynamics of resistant pathogens. Here, we show that the susceptibility of the gram-positive bacterium Listeria monocytogenes to the antibiotic fosfomycin is a complex trait involving interactions between resistance and virulence genes and the environment. We found that a FosX enzyme encoded in the listerial core genome confers intrinsic fosfomycin resistance to both pathogenic and non-pathogenic Listeria spp. However, in the genomic context of the pathogenic L. monocytogenes, FosX-mediated resistance is epistatically suppressed by two members of the PrfA virulence regulon, hpt and prfA, which upon activation by host signals induce increased fosfomycin influx into the bacterial cell. Consequently, in infection conditions, most L. monocytogenes isolates become susceptible to fosfomycin despite possessing a gene that confers high-level resistance to the drug. Our study establishes the molecular basis of an epistatic interaction between virulence and resistance genes controlling bacterial susceptibility to an antibiotic. The reported findings provide the rationale for the introduction of fosfomycin in the treatment of Listeria infections even though these bacteria are intrinsically resistant to the antibiotic in vitro.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Scortti</LastName>
<ForeName>Mariela</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Microbial Pathogenesis Group, Division of Infection Medicine, Edinburgh Medical School (Biomedical Sciences), University of Edinburgh, Little France campus, Edinburgh, United Kingdom.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Division of Infection & Immunity, The Roslin Institute, University of Edinburgh, Easter Bush campus, Edinburgh, United Kingdom.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Han</LastName>
<ForeName>Lei</ForeName>
<Initials>L</Initials>
<AffiliationInfo><Affiliation>Microbial Pathogenesis Group, Division of Infection Medicine, Edinburgh Medical School (Biomedical Sciences), University of Edinburgh, Little France campus, Edinburgh, United Kingdom.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Alvarez</LastName>
<ForeName>Sonsiray</ForeName>
<Initials>S</Initials>
<AffiliationInfo><Affiliation>Microbial Pathogenesis Group, Division of Infection Medicine, Edinburgh Medical School (Biomedical Sciences), University of Edinburgh, Little France campus, Edinburgh, United Kingdom.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Leclercq</LastName>
<ForeName>Alexandre</ForeName>
<Initials>A</Initials>
<Identifier Source="ORCID">0000-0003-3778-7313</Identifier>
<AffiliationInfo><Affiliation>Institut Pasteur, Biology of Infection Unit, INSERM U111 and National Reference Centre / WHO Collaborating Centre for Listeria, Paris, France.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Moura</LastName>
<ForeName>Alexandra</ForeName>
<Initials>A</Initials>
<Identifier Source="ORCID">0000-0003-0339-1230</Identifier>
<AffiliationInfo><Affiliation>Institut Pasteur, Biology of Infection Unit, INSERM U111 and National Reference Centre / WHO Collaborating Centre for Listeria, Paris, France.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Lecuit</LastName>
<ForeName>Marc</ForeName>
<Initials>M</Initials>
<Identifier Source="ORCID">0000-0002-4491-1063</Identifier>
<AffiliationInfo><Affiliation>Institut Pasteur, Biology of Infection Unit, INSERM U111 and National Reference Centre / WHO Collaborating Centre for Listeria, Paris, France.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Paris Descartes University, Division of Infectious Diseases and Tropical Medicine, Necker-Enfants Malades University Hospital, Paris, France.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Vazquez-Boland</LastName>
<ForeName>Jose</ForeName>
<Initials>J</Initials>
<Identifier Source="ORCID">0000-0003-4521-5972</Identifier>
<AffiliationInfo><Affiliation>Microbial Pathogenesis Group, Division of Infection Medicine, Edinburgh Medical School (Biomedical Sciences), University of Edinburgh, Little France campus, Edinburgh, United Kingdom.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Division of Infection & Immunity, The Roslin Institute, University of Edinburgh, Easter Bush campus, Edinburgh, United Kingdom.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<GrantList CompleteYN="Y"><Grant><GrantID>WT074020MA</GrantID>
<Agency>Wellcome Trust</Agency>
<Country>United Kingdom</Country>
</Grant>
<Grant><GrantID>BB/J004227/1</GrantID>
<Agency>Biotechnology and Biological Sciences Research Council</Agency>
<Country>United Kingdom</Country>
</Grant>
</GrantList>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
<PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2018</Year>
<Month>09</Month>
<Day>04</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>United States</Country>
<MedlineTA>PLoS Genet</MedlineTA>
<NlmUniqueID>101239074</NlmUniqueID>
<ISSNLinking>1553-7390</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D000900">Anti-Bacterial Agents</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D001426">Bacterial Proteins</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C451411">Hpt permease, Listeria monocytogenes</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D026901">Membrane Transport Proteins</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D010454">Peptide Termination Factors</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C545356">PrfA protein, Listeria monocytogenes</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>2N81MY12TE</RegistryNumber>
<NameOfSubstance UI="D005578">Fosfomycin</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.5.1.18</RegistryNumber>
<NameOfSubstance UI="D005982">Glutathione Transferase</NameOfSubstance>
</Chemical>
</ChemicalList>
<CitationSubset>IM</CitationSubset>
<CommentsCorrectionsList><CommentsCorrections RefType="ErratumIn"><RefSource>PLoS Genet. 2018 Oct 15;14(10):e1007727</RefSource>
<PMID Version="1">30321174</PMID>
</CommentsCorrections>
</CommentsCorrectionsList>
<MeshHeadingList><MeshHeading><DescriptorName UI="D000900" MajorTopicYN="N">Anti-Bacterial Agents</DescriptorName>
<QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName>
<QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D001426" MajorTopicYN="N">Bacterial Proteins</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D024881" MajorTopicYN="N">Drug Resistance, Bacterial</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D004843" MajorTopicYN="N">Epistasis, Genetic</DescriptorName>
<QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D005578" MajorTopicYN="N">Fosfomycin</DescriptorName>
<QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName>
<QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015964" MajorTopicYN="N">Gene Expression Regulation, Bacterial</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
<QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D005982" MajorTopicYN="N">Glutathione Transferase</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008089" MajorTopicYN="N">Listeria monocytogenes</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
<QualifierName UI="Q000472" MajorTopicYN="N">pathogenicity</QualifierName>
<QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008088" MajorTopicYN="N">Listeriosis</DescriptorName>
<QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName>
<QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D026901" MajorTopicYN="N">Membrane Transport Proteins</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D010454" MajorTopicYN="N">Peptide Termination Factors</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D018085" MajorTopicYN="N">Regulon</DescriptorName>
<QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D014774" MajorTopicYN="N">Virulence</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
</MeshHeading>
</MeshHeadingList>
<CoiStatement>The authors have declared that no competing interests exist.</CoiStatement>
</MedlineCitation>
<PubmedData><History><PubMedPubDate PubStatus="received"><Year>2017</Year>
<Month>10</Month>
<Day>27</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="accepted"><Year>2018</Year>
<Month>06</Month>
<Day>29</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="entrez"><Year>2018</Year>
<Month>9</Month>
<Day>5</Day>
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Epistatic control of intrinsic resistance by virulence genes in Listeria.

Epistatic control of intrinsic resistance by virulence genes in Listeria.

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