RapamycinFungusV1, Main, Exploration, bibRecord, 000984

The effector AWR5 from the plant pathogen Ralstonia solanacearum is an inhibitor of the TOR signalling pathway.

Identifieur interne : 000984 ( Main/Exploration ); précédent : 000983; suivant : 000985

The effector AWR5 from the plant pathogen Ralstonia solanacearum is an inhibitor of the TOR signalling pathway.

Auteurs : Crina Popa [Espagne] ; Liang Li [Espagne] ; Sergio Gil [Espagne] ; Laura Tatjer [Espagne] ; Keisuke Hashii [Japon] ; Mitsuaki Tabuchi [Japon] ; Núria S. Coll [Espagne] ; Joaquín Ari O [Espagne] ; Marc Valls [Espagne]

Source :

Scientific reports [ 2045-2322 ] ; 2016.

RBID : pubmed:27257085

Descripteurs français

KwdFr :
- Autophagie (MeSH), Inhibiteurs de protéines kinases (pharmacologie), Interactions hôte-pathogène (MeSH), Maladies des plantes (microbiologie), Protéines bactériennes (biosynthèse), Protéines bactériennes (génétique), Protéines de Saccharomyces cerevisiae (métabolisme), Protéines végétales (physiologie), Ralstonia solanacearum (génétique), Ralstonia solanacearum (métabolisme), Saccharomyces cerevisiae (croissance et développement), Saccharomyces cerevisiae (génétique), Saccharomyces cerevisiae (métabolisme), Sirolimus (pharmacologie), Sérine-thréonine kinases TOR (physiologie), Tabac (microbiologie), Transcriptome (MeSH), Transduction du signal (MeSH).
MESH :
- biosynthèse : Protéines bactériennes.
- croissance et développement : Saccharomyces cerevisiae.
- génétique : Protéines bactériennes, Ralstonia solanacearum, Saccharomyces cerevisiae.
- microbiologie : Maladies des plantes, Tabac.
- métabolisme : Protéines de Saccharomyces cerevisiae, Ralstonia solanacearum, Saccharomyces cerevisiae.
- pharmacologie : Inhibiteurs de protéines kinases, Sirolimus.
- physiologie : Protéines végétales, Sérine-thréonine kinases TOR.
- Autophagie, Interactions hôte-pathogène, Transcriptome, Transduction du signal.

English descriptors

KwdEn :
- Autophagy (MeSH), Bacterial Proteins (biosynthesis), Bacterial Proteins (genetics), Host-Pathogen Interactions (MeSH), Plant Diseases (microbiology), Plant Proteins (physiology), Protein Kinase Inhibitors (pharmacology), Ralstonia solanacearum (genetics), Ralstonia solanacearum (metabolism), Saccharomyces cerevisiae (genetics), Saccharomyces cerevisiae (growth & development), Saccharomyces cerevisiae (metabolism), Saccharomyces cerevisiae Proteins (metabolism), Signal Transduction (MeSH), Sirolimus (pharmacology), TOR Serine-Threonine Kinases (physiology), Tobacco (microbiology), Transcriptome (MeSH).
MESH :
- chemical , biosynthesis : Bacterial Proteins.
- chemical , genetics : Bacterial Proteins.
- genetics : Ralstonia solanacearum, Saccharomyces cerevisiae.
- growth & development : Saccharomyces cerevisiae.
- metabolism : Ralstonia solanacearum, Saccharomyces cerevisiae, Saccharomyces cerevisiae Proteins.
- microbiology : Plant Diseases, Tobacco.
- chemical , pharmacology : Protein Kinase Inhibitors, Sirolimus.
- chemical , physiology : Plant Proteins, TOR Serine-Threonine Kinases.
- Autophagy, Host-Pathogen Interactions, Signal Transduction, Transcriptome.

Abstract

Bacterial pathogens possess complex type III effector (T3E) repertoires that are translocated inside the host cells to cause disease. However, only a minor proportion of these effectors have been assigned a function. Here, we show that the T3E AWR5 from the phytopathogen Ralstonia solanacearum is an inhibitor of TOR, a central regulator in eukaryotes that controls the switch between cell growth and stress responses in response to nutrient availability. Heterologous expression of AWR5 in yeast caused growth inhibition and autophagy induction coupled to massive transcriptomic changes, unmistakably reminiscent of TOR inhibition by rapamycin or nitrogen starvation. Detailed genetic analysis of these phenotypes in yeast, including suppression of AWR5-induced toxicity by mutation of CDC55 and TPD3, encoding regulatory subunits of the PP2A phosphatase, indicated that AWR5 might exert its function by directly or indirectly inhibiting the TOR pathway upstream PP2A. We present evidence in planta that this T3E caused a decrease in TOR-regulated plant nitrate reductase activity and also that normal levels of TOR and the Cdc55 homologues in plants are required for R. solanacearum virulence. Our results suggest that the TOR pathway is a bona fide T3E target and further prove that yeast is a useful platform for T3E function characterisation.

DOI: 10.1038/srep27058
PubMed: 27257085
PubMed Central: PMC4891724

Affiliations:

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

to stream Main, to step Corpus: 000A40
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Le document en format XML

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<term>Host-Pathogen Interactions (MeSH)</term>
<term>Plant Diseases (microbiology)</term>
<term>Plant Proteins (physiology)</term>
<term>Protein Kinase Inhibitors (pharmacology)</term>
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<term>Tobacco (microbiology)</term>
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<term>Interactions hôte-pathogène (MeSH)</term>
<term>Maladies des plantes (microbiologie)</term>
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<term>Saccharomyces cerevisiae</term>
<term>Saccharomyces cerevisiae Proteins</term>
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<term>Transcriptome</term>
</keywords>
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<term>Interactions hôte-pathogène</term>
<term>Transcriptome</term>
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<front><div type="abstract" xml:lang="en">Bacterial pathogens possess complex type III effector (T3E) repertoires that are translocated inside the host cells to cause disease. However, only a minor proportion of these effectors have been assigned a function. Here, we show that the T3E AWR5 from the phytopathogen Ralstonia solanacearum is an inhibitor of TOR, a central regulator in eukaryotes that controls the switch between cell growth and stress responses in response to nutrient availability. Heterologous expression of AWR5 in yeast caused growth inhibition and autophagy induction coupled to massive transcriptomic changes, unmistakably reminiscent of TOR inhibition by rapamycin or nitrogen starvation. Detailed genetic analysis of these phenotypes in yeast, including suppression of AWR5-induced toxicity by mutation of CDC55 and TPD3, encoding regulatory subunits of the PP2A phosphatase, indicated that AWR5 might exert its function by directly or indirectly inhibiting the TOR pathway upstream PP2A. We present evidence in planta that this T3E caused a decrease in TOR-regulated plant nitrate reductase activity and also that normal levels of TOR and the Cdc55 homologues in plants are required for R. solanacearum virulence. Our results suggest that the TOR pathway is a bona fide T3E target and further prove that yeast is a useful platform for T3E function characterisation.</div>
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<ISOAbbreviation>Sci Rep</ISOAbbreviation>
</Journal>
<ArticleTitle>The effector AWR5 from the plant pathogen Ralstonia solanacearum is an inhibitor of the TOR signalling pathway.</ArticleTitle>
<Pagination><MedlinePgn>27058</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1038/srep27058</ELocationID>
<Abstract><AbstractText>Bacterial pathogens possess complex type III effector (T3E) repertoires that are translocated inside the host cells to cause disease. However, only a minor proportion of these effectors have been assigned a function. Here, we show that the T3E AWR5 from the phytopathogen Ralstonia solanacearum is an inhibitor of TOR, a central regulator in eukaryotes that controls the switch between cell growth and stress responses in response to nutrient availability. Heterologous expression of AWR5 in yeast caused growth inhibition and autophagy induction coupled to massive transcriptomic changes, unmistakably reminiscent of TOR inhibition by rapamycin or nitrogen starvation. Detailed genetic analysis of these phenotypes in yeast, including suppression of AWR5-induced toxicity by mutation of CDC55 and TPD3, encoding regulatory subunits of the PP2A phosphatase, indicated that AWR5 might exert its function by directly or indirectly inhibiting the TOR pathway upstream PP2A. We present evidence in planta that this T3E caused a decrease in TOR-regulated plant nitrate reductase activity and also that normal levels of TOR and the Cdc55 homologues in plants are required for R. solanacearum virulence. Our results suggest that the TOR pathway is a bona fide T3E target and further prove that yeast is a useful platform for T3E function characterisation.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Popa</LastName>
<ForeName>Crina</ForeName>
<Initials>C</Initials>
<AffiliationInfo><Affiliation>Centre for Research in Agricultural Genomics (CSIC-IRTA-UAB-UB), Bellaterra, Catalonia, Spain.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Genetics Department, Universitat de Barcelona, Barcelona, Catalonia, Spain.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Li</LastName>
<ForeName>Liang</ForeName>
<Initials>L</Initials>
<AffiliationInfo><Affiliation>Centre for Research in Agricultural Genomics (CSIC-IRTA-UAB-UB), Bellaterra, Catalonia, Spain.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Gil</LastName>
<ForeName>Sergio</ForeName>
<Initials>S</Initials>
<AffiliationInfo><Affiliation>Genetics Department, Universitat de Barcelona, Barcelona, Catalonia, Spain.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Tatjer</LastName>
<ForeName>Laura</ForeName>
<Initials>L</Initials>
<AffiliationInfo><Affiliation>Institut de Biotecnologia i Biomedicina and Departament de Bioquímica i Biologia Molecular, Universitat Autònoma de Barcelona, Cerdanyola del Vallès, Catalonia, Spain.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Hashii</LastName>
<ForeName>Keisuke</ForeName>
<Initials>K</Initials>
<AffiliationInfo><Affiliation>Laboratory of Applied Molecular and Cell Biology, Kagawa University, Kagawa, Japan.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Tabuchi</LastName>
<ForeName>Mitsuaki</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Laboratory of Applied Molecular and Cell Biology, Kagawa University, Kagawa, Japan.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Coll</LastName>
<ForeName>Núria S</ForeName>
<Initials>NS</Initials>
<AffiliationInfo><Affiliation>Centre for Research in Agricultural Genomics (CSIC-IRTA-UAB-UB), Bellaterra, Catalonia, Spain.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Ariño</LastName>
<ForeName>Joaquín</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>Institut de Biotecnologia i Biomedicina and Departament de Bioquímica i Biologia Molecular, Universitat Autònoma de Barcelona, Cerdanyola del Vallès, Catalonia, Spain.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Valls</LastName>
<ForeName>Marc</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Centre for Research in Agricultural Genomics (CSIC-IRTA-UAB-UB), Bellaterra, Catalonia, Spain.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Genetics Department, Universitat de Barcelona, Barcelona, Catalonia, Spain.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
<PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2016</Year>
<Month>06</Month>
<Day>03</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>England</Country>
<MedlineTA>Sci Rep</MedlineTA>
<NlmUniqueID>101563288</NlmUniqueID>
<ISSNLinking>2045-2322</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D001426">Bacterial Proteins</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D010940">Plant Proteins</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D047428">Protein Kinase Inhibitors</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D029701">Saccharomyces cerevisiae Proteins</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.1.1</RegistryNumber>
<NameOfSubstance UI="D058570">TOR Serine-Threonine Kinases</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>W36ZG6FT64</RegistryNumber>
<NameOfSubstance UI="D020123">Sirolimus</NameOfSubstance>
</Chemical>
</ChemicalList>
<CitationSubset>IM</CitationSubset>
<MeshHeadingList><MeshHeading><DescriptorName UI="D001343" MajorTopicYN="N">Autophagy</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D001426" MajorTopicYN="N">Bacterial Proteins</DescriptorName>
<QualifierName UI="Q000096" MajorTopicYN="N">biosynthesis</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D054884" MajorTopicYN="N">Host-Pathogen Interactions</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D010935" MajorTopicYN="N">Plant Diseases</DescriptorName>
<QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D010940" MajorTopicYN="N">Plant Proteins</DescriptorName>
<QualifierName UI="Q000502" MajorTopicYN="N">physiology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D047428" MajorTopicYN="N">Protein Kinase Inhibitors</DescriptorName>
<QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D043368" MajorTopicYN="N">Ralstonia solanacearum</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D012441" MajorTopicYN="N">Saccharomyces cerevisiae</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000254" MajorTopicYN="N">growth & development</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D029701" MajorTopicYN="N">Saccharomyces cerevisiae Proteins</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D020123" MajorTopicYN="N">Sirolimus</DescriptorName>
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<MeshHeading><DescriptorName UI="D058570" MajorTopicYN="N">TOR Serine-Threonine Kinases</DescriptorName>
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<QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D059467" MajorTopicYN="N">Transcriptome</DescriptorName>
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	Serveur d'exploration sur la rapamycine et les champignons
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The effector AWR5 from the plant pathogen Ralstonia solanacearum is an inhibitor of the TOR signalling pathway.

The effector AWR5 from the plant pathogen Ralstonia solanacearum is an inhibitor of the TOR signalling pathway.

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