RapamycinFungusV1, Main, Exploration, bibRecord, 000D58

A conserved mechanism of TOR-dependent RCK-mediated mRNA degradation regulates autophagy.

Identifieur interne : 000D58 ( Main/Exploration ); précédent : 000D57; suivant : 000D59

A conserved mechanism of TOR-dependent RCK-mediated mRNA degradation regulates autophagy.

Auteurs : Guowu Hu ; Travis Mcquiston ; Amélie Bernard ; Yoon-Dong Park ; Jin Qiu ; Ali Vural ; Nannan Zhang ; Scott R. Waterman ; Nathan H. Blewett [États-Unis] ; Timothy G. Myers ; Richard J. Maraia [États-Unis] ; John H. Kehrl ; Gulbu Uzel ; Daniel J. Klionsky ; Peter R. Williamson

Source :

Nature cell biology [ 1476-4679 ] ; 2015.

RBID : pubmed:26098573

Descripteurs français

English descriptors

Abstract

Autophagy is an essential eukaryotic pathway requiring tight regulation to maintain homeostasis and preclude disease. Using yeast and mammalian cells, we report a conserved mechanism of autophagy regulation by RNA helicase RCK family members in association with the decapping enzyme Dcp2. Under nutrient-replete conditions, Dcp2 undergoes TOR-dependent phosphorylation and associates with RCK members to form a complex with autophagy-related (ATG) mRNA transcripts, leading to decapping, degradation and autophagy suppression. Simultaneous with the induction of ATG mRNA synthesis, starvation reverses the process, facilitating ATG mRNA accumulation and autophagy induction. This conserved post-transcriptional mechanism modulates fungal virulence and the mammalian inflammasome, the latter providing mechanistic insight into autoimmunity reported in a patient with a PIK3CD/p110δ gain-of-function mutation. We propose a dynamic model wherein RCK family members, in conjunction with Dcp2, function in controlling ATG mRNA stability to govern autophagy, which in turn modulates vital cellular processes affecting inflammation and microbial pathogenesis.

DOI: 10.1038/ncb3189
PubMed: 26098573
PubMed Central: PMC4528364

Affiliations:

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Le document en format XML

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<author><name sortKey="Hu, Guowu" sort="Hu, Guowu" uniqKey="Hu G" first="Guowu" last="Hu">Guowu Hu</name>
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<series><title level="j">Nature cell biology</title>
<idno type="eISSN">1476-4679</idno>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term>
<term>Autoimmunity (genetics)</term>
<term>Autophagy (genetics)</term>
<term>Cell Line, Tumor (MeSH)</term>
<term>Cells, Cultured (MeSH)</term>
<term>Class Ia Phosphatidylinositol 3-Kinase (genetics)</term>
<term>Class Ia Phosphatidylinositol 3-Kinase (metabolism)</term>
<term>Cryptococcus neoformans (genetics)</term>
<term>Cryptococcus neoformans (metabolism)</term>
<term>DEAD-box RNA Helicases (genetics)</term>
<term>DEAD-box RNA Helicases (metabolism)</term>
<term>Endoribonucleases (genetics)</term>
<term>Endoribonucleases (metabolism)</term>
<term>Female (MeSH)</term>
<term>Gene Expression Regulation, Fungal (MeSH)</term>
<term>HeLa Cells (MeSH)</term>
<term>Humans (MeSH)</term>
<term>Immunoblotting (MeSH)</term>
<term>Inflammasomes (genetics)</term>
<term>Inflammasomes (metabolism)</term>
<term>Mice, Inbred C57BL (MeSH)</term>
<term>Mutation (MeSH)</term>
<term>Phosphorylation (MeSH)</term>
<term>Protein-Serine-Threonine Kinases (metabolism)</term>
<term>RNA Stability (genetics)</term>
<term>RNA, Messenger (genetics)</term>
<term>RNA, Messenger (metabolism)</term>
<term>Reverse Transcriptase Polymerase Chain Reaction (MeSH)</term>
<term>Saccharomyces cerevisiae (genetics)</term>
<term>Saccharomyces cerevisiae (metabolism)</term>
<term>Saccharomyces cerevisiae Proteins (genetics)</term>
<term>Saccharomyces cerevisiae Proteins (metabolism)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>ARN messager (génétique)</term>
<term>ARN messager (métabolisme)</term>
<term>Animaux (MeSH)</term>
<term>Auto-immunité (génétique)</term>
<term>Autophagie (génétique)</term>
<term>Cellules HeLa (MeSH)</term>
<term>Cellules cultivées (MeSH)</term>
<term>Cryptococcus neoformans (génétique)</term>
<term>Cryptococcus neoformans (métabolisme)</term>
<term>DEAD-box RNA helicases (génétique)</term>
<term>DEAD-box RNA helicases (métabolisme)</term>
<term>Endoribonucleases (génétique)</term>
<term>Endoribonucleases (métabolisme)</term>
<term>Femelle (MeSH)</term>
<term>Humains (MeSH)</term>
<term>Immunotransfert (MeSH)</term>
<term>Inflammasomes (génétique)</term>
<term>Inflammasomes (métabolisme)</term>
<term>Lignée cellulaire tumorale (MeSH)</term>
<term>Mutation (MeSH)</term>
<term>Phosphatidylinositol 3-kinase de classe Ia (génétique)</term>
<term>Phosphatidylinositol 3-kinase de classe Ia (métabolisme)</term>
<term>Phosphorylation (MeSH)</term>
<term>Protein-Serine-Threonine Kinases (métabolisme)</term>
<term>Protéines de Saccharomyces cerevisiae (génétique)</term>
<term>Protéines de Saccharomyces cerevisiae (métabolisme)</term>
<term>RT-PCR (MeSH)</term>
<term>Régulation de l'expression des gènes fongiques (MeSH)</term>
<term>Saccharomyces cerevisiae (génétique)</term>
<term>Saccharomyces cerevisiae (métabolisme)</term>
<term>Souris de lignée C57BL (MeSH)</term>
<term>Stabilité de l'ARN (génétique)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Class Ia Phosphatidylinositol 3-Kinase</term>
<term>DEAD-box RNA Helicases</term>
<term>Endoribonucleases</term>
<term>Inflammasomes</term>
<term>RNA, Messenger</term>
<term>Saccharomyces cerevisiae Proteins</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Autoimmunity</term>
<term>Autophagy</term>
<term>Cryptococcus neoformans</term>
<term>RNA Stability</term>
<term>Saccharomyces cerevisiae</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>ARN messager</term>
<term>Auto-immunité</term>
<term>Autophagie</term>
<term>Cryptococcus neoformans</term>
<term>DEAD-box RNA helicases</term>
<term>Endoribonucleases</term>
<term>Inflammasomes</term>
<term>Phosphatidylinositol 3-kinase de classe Ia</term>
<term>Protéines de Saccharomyces cerevisiae</term>
<term>Saccharomyces cerevisiae</term>
<term>Stabilité de l'ARN</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Class Ia Phosphatidylinositol 3-Kinase</term>
<term>Cryptococcus neoformans</term>
<term>DEAD-box RNA Helicases</term>
<term>Endoribonucleases</term>
<term>Inflammasomes</term>
<term>Protein-Serine-Threonine Kinases</term>
<term>RNA, Messenger</term>
<term>Saccharomyces cerevisiae</term>
<term>Saccharomyces cerevisiae Proteins</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>ARN messager</term>
<term>Cryptococcus neoformans</term>
<term>DEAD-box RNA helicases</term>
<term>Endoribonucleases</term>
<term>Inflammasomes</term>
<term>Phosphatidylinositol 3-kinase de classe Ia</term>
<term>Protein-Serine-Threonine Kinases</term>
<term>Protéines de Saccharomyces cerevisiae</term>
<term>Saccharomyces cerevisiae</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Cell Line, Tumor</term>
<term>Cells, Cultured</term>
<term>Female</term>
<term>Gene Expression Regulation, Fungal</term>
<term>HeLa Cells</term>
<term>Humans</term>
<term>Immunoblotting</term>
<term>Mice, Inbred C57BL</term>
<term>Mutation</term>
<term>Phosphorylation</term>
<term>Reverse Transcriptase Polymerase Chain Reaction</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Cellules HeLa</term>
<term>Cellules cultivées</term>
<term>Femelle</term>
<term>Humains</term>
<term>Immunotransfert</term>
<term>Lignée cellulaire tumorale</term>
<term>Mutation</term>
<term>Phosphorylation</term>
<term>RT-PCR</term>
<term>Régulation de l'expression des gènes fongiques</term>
<term>Souris de lignée C57BL</term>
</keywords>
</textClass>
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<front><div type="abstract" xml:lang="en">Autophagy is an essential eukaryotic pathway requiring tight regulation to maintain homeostasis and preclude disease. Using yeast and mammalian cells, we report a conserved mechanism of autophagy regulation by RNA helicase RCK family members in association with the decapping enzyme Dcp2. Under nutrient-replete conditions, Dcp2 undergoes TOR-dependent phosphorylation and associates with RCK members to form a complex with autophagy-related (ATG) mRNA transcripts, leading to decapping, degradation and autophagy suppression. Simultaneous with the induction of ATG mRNA synthesis, starvation reverses the process, facilitating ATG mRNA accumulation and autophagy induction. This conserved post-transcriptional mechanism modulates fungal virulence and the mammalian inflammasome, the latter providing mechanistic insight into autoimmunity reported in a patient with a PIK3CD/p110δ gain-of-function mutation. We propose a dynamic model wherein RCK family members, in conjunction with Dcp2, function in controlling ATG mRNA stability to govern autophagy, which in turn modulates vital cellular processes affecting inflammation and microbial pathogenesis. </div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">26098573</PMID>
<DateCompleted><Year>2015</Year>
<Month>09</Month>
<Day>29</Day>
</DateCompleted>
<DateRevised><Year>2019</Year>
<Month>10</Month>
<Day>08</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1476-4679</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>17</Volume>
<Issue>7</Issue>
<PubDate><Year>2015</Year>
<Month>Jul</Month>
</PubDate>
</JournalIssue>
<Title>Nature cell biology</Title>
<ISOAbbreviation>Nat Cell Biol</ISOAbbreviation>
</Journal>
<ArticleTitle>A conserved mechanism of TOR-dependent RCK-mediated mRNA degradation regulates autophagy.</ArticleTitle>
<Pagination><MedlinePgn>930-942</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1038/ncb3189</ELocationID>
<Abstract><AbstractText>Autophagy is an essential eukaryotic pathway requiring tight regulation to maintain homeostasis and preclude disease. Using yeast and mammalian cells, we report a conserved mechanism of autophagy regulation by RNA helicase RCK family members in association with the decapping enzyme Dcp2. Under nutrient-replete conditions, Dcp2 undergoes TOR-dependent phosphorylation and associates with RCK members to form a complex with autophagy-related (ATG) mRNA transcripts, leading to decapping, degradation and autophagy suppression. Simultaneous with the induction of ATG mRNA synthesis, starvation reverses the process, facilitating ATG mRNA accumulation and autophagy induction. This conserved post-transcriptional mechanism modulates fungal virulence and the mammalian inflammasome, the latter providing mechanistic insight into autoimmunity reported in a patient with a PIK3CD/p110δ gain-of-function mutation. We propose a dynamic model wherein RCK family members, in conjunction with Dcp2, function in controlling ATG mRNA stability to govern autophagy, which in turn modulates vital cellular processes affecting inflammation and microbial pathogenesis. </AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y" EqualContrib="Y"><LastName>Hu</LastName>
<ForeName>Guowu</ForeName>
<Initials>G</Initials>
<AffiliationInfo><Affiliation>Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA, 20892.</Affiliation>
</AffiliationInfo>
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<AffiliationInfo><Affiliation>Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA, 20892.</Affiliation>
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<AffiliationInfo><Affiliation>Life Sciences Institute, University of Michigan, Ann Arbor, MI, USA 48109.</Affiliation>
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<AffiliationInfo><Affiliation>Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA, 20892.</Affiliation>
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<AffiliationInfo><Affiliation>Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA, 20892.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Vural</LastName>
<ForeName>Ali</ForeName>
<Initials>A</Initials>
<AffiliationInfo><Affiliation>Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA, 20892.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Zhang</LastName>
<ForeName>Nannan</ForeName>
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<AffiliationInfo><Affiliation>Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA, 20892.</Affiliation>
</AffiliationInfo>
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<ForeName>Scott R</ForeName>
<Initials>SR</Initials>
<AffiliationInfo><Affiliation>Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA, 20892.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Blewett</LastName>
<ForeName>Nathan H</ForeName>
<Initials>NH</Initials>
<AffiliationInfo><Affiliation>Intramural Research Program in Genomics of Differentiation, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Myers</LastName>
<ForeName>Timothy G</ForeName>
<Initials>TG</Initials>
<AffiliationInfo><Affiliation>Genomic Technologies Section, Research Technologies Branch, National Institute of Allergy and Infectious Diseases, National Institutes of Health, MD, USA, 20892.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Maraia</LastName>
<ForeName>Richard J</ForeName>
<Initials>RJ</Initials>
<AffiliationInfo><Affiliation>Intramural Research Program in Genomics of Differentiation, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Kehrl</LastName>
<ForeName>John H</ForeName>
<Initials>JH</Initials>
<AffiliationInfo><Affiliation>Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA, 20892.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Uzel</LastName>
<ForeName>Gulbu</ForeName>
<Initials>G</Initials>
<AffiliationInfo><Affiliation>Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA, 20892.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Klionsky</LastName>
<ForeName>Daniel J</ForeName>
<Initials>DJ</Initials>
<AffiliationInfo><Affiliation>Life Sciences Institute, University of Michigan, Ann Arbor, MI, USA 48109.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Williamson</LastName>
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<Initials>PR</Initials>
<AffiliationInfo><Affiliation>Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA, 20892.</Affiliation>
</AffiliationInfo>
</Author>
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<Agency>NIGMS NIH HHS</Agency>
<Country>United States</Country>
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<Agency>Intramural NIH HHS</Agency>
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<Country>United States</Country>
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<Agency>Intramural NIH HHS</Agency>
<Country>United States</Country>
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<Agency>Intramural NIH HHS</Agency>
<Country>United States</Country>
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<Grant><GrantID>ZIA AI001124-01</GrantID>
<Agency>Intramural NIH HHS</Agency>
<Country>United States</Country>
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<Grant><GrantID>ZIA AI001123-05</GrantID>
<Agency>Intramural NIH HHS</Agency>
<Country>United States</Country>
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<Grant><GrantID>R01 GM088565</GrantID>
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<Agency>NIGMS NIH HHS</Agency>
<Country>United States</Country>
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<Month>06</Month>
<Day>22</Day>
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<MedlineTA>Nat Cell Biol</MedlineTA>
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<ISSNLinking>1465-7392</ISSNLinking>
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<NameOfSubstance UI="D012333">RNA, Messenger</NameOfSubstance>
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<MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
</MeshHeading>
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<MeshHeading><DescriptorName UI="D001343" MajorTopicYN="N">Autophagy</DescriptorName>
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</MeshHeading>
<MeshHeading><DescriptorName UI="D045744" MajorTopicYN="N">Cell Line, Tumor</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D002478" MajorTopicYN="N">Cells, Cultured</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D058543" MajorTopicYN="N">Class Ia Phosphatidylinositol 3-Kinase</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D003455" MajorTopicYN="N">Cryptococcus neoformans</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D053487" MajorTopicYN="N">DEAD-box RNA Helicases</DescriptorName>
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<MeshHeading><DescriptorName UI="D004722" MajorTopicYN="N">Endoribonucleases</DescriptorName>
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<MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015966" MajorTopicYN="N">Gene Expression Regulation, Fungal</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006367" MajorTopicYN="N">HeLa Cells</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015151" MajorTopicYN="N">Immunoblotting</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D058847" MajorTopicYN="N">Inflammasomes</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008810" MajorTopicYN="N">Mice, Inbred C57BL</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D009154" MajorTopicYN="N">Mutation</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D010766" MajorTopicYN="N">Phosphorylation</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D017346" MajorTopicYN="N">Protein-Serine-Threonine Kinases</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
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<MeshHeading><DescriptorName UI="D020871" MajorTopicYN="N">RNA Stability</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
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<MeshHeading><DescriptorName UI="D012333" MajorTopicYN="N">RNA, Messenger</DescriptorName>
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<MeshHeading><DescriptorName UI="D020133" MajorTopicYN="N">Reverse Transcriptase Polymerase Chain Reaction</DescriptorName>
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	Serveur d'exploration sur la rapamycine et les champignons
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A conserved mechanism of TOR-dependent RCK-mediated mRNA degradation regulates autophagy.

A conserved mechanism of TOR-dependent RCK-mediated mRNA degradation regulates autophagy.

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