RapamycinFungusV1, Main, Exploration, bibRecord, 001730

Efficient Tor signaling requires a functional class C Vps protein complex in Saccharomyces cerevisiae.

Identifieur interne : 001730 ( Main/Exploration ); précédent : 001729; suivant : 001731

Efficient Tor signaling requires a functional class C Vps protein complex in Saccharomyces cerevisiae.

Auteurs : Sara A. Zurita-Martinez [États-Unis] ; Rekha Puria ; Xuewen Pan ; Jef D. Boeke ; Maria E. Cardenas

Source :

Genetics [ 0016-6731 ] ; 2007.

RBID : pubmed:17565946

Descripteurs français

English descriptors

KwdEn :
- Adaptor Proteins, Vesicular Transport (MeSH), Amino Acids (pharmacology), Base Sequence (MeSH), Cell Cycle Proteins (genetics), Cell Cycle Proteins (metabolism), DNA Primers (genetics), DNA, Fungal (genetics), Genes, Fungal (MeSH), Membrane Proteins (genetics), Membrane Proteins (metabolism), Multiprotein Complexes (MeSH), Mutation (MeSH), Phosphatidylinositol 3-Kinases (genetics), Phosphatidylinositol 3-Kinases (metabolism), Phosphotransferases (Alcohol Group Acceptor) (genetics), Phosphotransferases (Alcohol Group Acceptor) (metabolism), Protein-Serine-Threonine Kinases (MeSH), Saccharomyces cerevisiae (drug effects), Saccharomyces cerevisiae (genetics), Saccharomyces cerevisiae (metabolism), Saccharomyces cerevisiae Proteins (chemistry), Saccharomyces cerevisiae Proteins (classification), Saccharomyces cerevisiae Proteins (genetics), Saccharomyces cerevisiae Proteins (metabolism), Signal Transduction (MeSH), Vesicular Transport Proteins (MeSH).
MESH :
- chemical , chemistry : Saccharomyces cerevisiae Proteins.
- chemical , classification : Saccharomyces cerevisiae Proteins.
- chemical , genetics : Cell Cycle Proteins, DNA Primers, DNA, Fungal, Membrane Proteins, Phosphatidylinositol 3-Kinases, Phosphotransferases (Alcohol Group Acceptor), Saccharomyces cerevisiae Proteins.
- chemical , metabolism : Cell Cycle Proteins, Membrane Proteins, Phosphatidylinositol 3-Kinases, Phosphotransferases (Alcohol Group Acceptor), Saccharomyces cerevisiae Proteins.
- chemical , pharmacology : Amino Acids.
- chemical : Adaptor Proteins, Vesicular Transport, Multiprotein Complexes, Protein-Serine-Threonine Kinases, Vesicular Transport Proteins.
- drug effects : Saccharomyces cerevisiae.
- genetics : Saccharomyces cerevisiae.
- metabolism : Saccharomyces cerevisiae.
- Base Sequence, Genes, Fungal, Mutation, Signal Transduction.

Abstract

The Tor kinases regulate responses to nutrients and control cell growth. Unlike most organisms that only contain one Tor protein, Saccharomyces cerevisiae expresses two, Tor1 and Tor2, which are thought to share all of the rapamycin-sensitive functions attributable to Tor signaling. Here we conducted a genetic screen that defined the global TOR1 synthetic fitness or lethal interaction gene network. This screen identified mutations in distinctive functional categories that impaired vacuolar function, including components of the EGO/Gse and PAS complexes that reduce fitness. In addition, tor1 is lethal in combination with mutations in class C Vps complex components. We find that Tor1 does not regulate the known function of the class C Vps complex in protein sorting. Instead class C vps mutants fail to recover from rapamycin-induced growth arrest or to survive nitrogen starvation and have low levels of amino acids. Remarkably, addition of glutamate or glutamine restores viability to a tor1 pep3 mutant strain. We conclude that Tor1 is more effective than Tor2 at providing rapamycin-sensitive Tor signaling under conditions of amino acid limitation, and that an intact class C Vps complex is required to mediate intracellular amino acid homeostasis for efficient Tor signaling.

DOI: 10.1534/genetics.107.072835
PubMed: 17565946
PubMed Central: PMC1950620

Affiliations:

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

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to stream Main, to step Curation: 001696

Le document en format XML

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<term>Cell Cycle Proteins (genetics)</term>
<term>Cell Cycle Proteins (metabolism)</term>
<term>DNA Primers (genetics)</term>
<term>DNA, Fungal (genetics)</term>
<term>Genes, Fungal (MeSH)</term>
<term>Membrane Proteins (genetics)</term>
<term>Membrane Proteins (metabolism)</term>
<term>Multiprotein Complexes (MeSH)</term>
<term>Mutation (MeSH)</term>
<term>Phosphatidylinositol 3-Kinases (genetics)</term>
<term>Phosphatidylinositol 3-Kinases (metabolism)</term>
<term>Phosphotransferases (Alcohol Group Acceptor) (genetics)</term>
<term>Phosphotransferases (Alcohol Group Acceptor) (metabolism)</term>
<term>Protein-Serine-Threonine Kinases (MeSH)</term>
<term>Saccharomyces cerevisiae (drug effects)</term>
<term>Saccharomyces cerevisiae (genetics)</term>
<term>Saccharomyces cerevisiae (metabolism)</term>
<term>Saccharomyces cerevisiae Proteins (chemistry)</term>
<term>Saccharomyces cerevisiae Proteins (classification)</term>
<term>Saccharomyces cerevisiae Proteins (genetics)</term>
<term>Saccharomyces cerevisiae Proteins (metabolism)</term>
<term>Signal Transduction (MeSH)</term>
<term>Vesicular Transport Proteins (MeSH)</term>
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<term>Acides aminés (pharmacologie)</term>
<term>Amorces ADN (génétique)</term>
<term>Complexes multiprotéiques (MeSH)</term>
<term>Gènes fongiques (MeSH)</term>
<term>Mutation (MeSH)</term>
<term>Phosphatidylinositol 3-kinases (génétique)</term>
<term>Phosphatidylinositol 3-kinases (métabolisme)</term>
<term>Phosphotransferases (Alcohol Group Acceptor) (génétique)</term>
<term>Phosphotransferases (Alcohol Group Acceptor) (métabolisme)</term>
<term>Protein-Serine-Threonine Kinases (MeSH)</term>
<term>Protéines adaptatrices du transport vésiculaire (MeSH)</term>
<term>Protéines de Saccharomyces cerevisiae (classification)</term>
<term>Protéines de Saccharomyces cerevisiae (composition chimique)</term>
<term>Protéines de Saccharomyces cerevisiae (génétique)</term>
<term>Protéines de Saccharomyces cerevisiae (métabolisme)</term>
<term>Protéines du cycle cellulaire (génétique)</term>
<term>Protéines du cycle cellulaire (métabolisme)</term>
<term>Protéines du transport vésiculaire (MeSH)</term>
<term>Protéines membranaires (génétique)</term>
<term>Protéines membranaires (métabolisme)</term>
<term>Saccharomyces cerevisiae (effets des médicaments et des substances chimiques)</term>
<term>Saccharomyces cerevisiae (génétique)</term>
<term>Saccharomyces cerevisiae (métabolisme)</term>
<term>Séquence nucléotidique (MeSH)</term>
<term>Transduction du signal (MeSH)</term>
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<term>Membrane Proteins</term>
<term>Phosphatidylinositol 3-Kinases</term>
<term>Phosphotransferases (Alcohol Group Acceptor)</term>
<term>Saccharomyces cerevisiae Proteins</term>
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<term>Protein-Serine-Threonine Kinases</term>
<term>Vesicular Transport Proteins</term>
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<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Saccharomyces cerevisiae</term>
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<term>Phosphotransferases (Alcohol Group Acceptor)</term>
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<term>Protéines du cycle cellulaire</term>
<term>Protéines membranaires</term>
<term>Saccharomyces cerevisiae</term>
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<term>Phosphotransferases (Alcohol Group Acceptor)</term>
<term>Protéines de Saccharomyces cerevisiae</term>
<term>Protéines du cycle cellulaire</term>
<term>Protéines membranaires</term>
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<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Acides aminés</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Base Sequence</term>
<term>Genes, Fungal</term>
<term>Mutation</term>
<term>Signal Transduction</term>
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<term>Gènes fongiques</term>
<term>Mutation</term>
<term>Protein-Serine-Threonine Kinases</term>
<term>Protéines adaptatrices du transport vésiculaire</term>
<term>Protéines du transport vésiculaire</term>
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<front><div type="abstract" xml:lang="en">The Tor kinases regulate responses to nutrients and control cell growth. Unlike most organisms that only contain one Tor protein, Saccharomyces cerevisiae expresses two, Tor1 and Tor2, which are thought to share all of the rapamycin-sensitive functions attributable to Tor signaling. Here we conducted a genetic screen that defined the global TOR1 synthetic fitness or lethal interaction gene network. This screen identified mutations in distinctive functional categories that impaired vacuolar function, including components of the EGO/Gse and PAS complexes that reduce fitness. In addition, tor1 is lethal in combination with mutations in class C Vps complex components. We find that Tor1 does not regulate the known function of the class C Vps complex in protein sorting. Instead class C vps mutants fail to recover from rapamycin-induced growth arrest or to survive nitrogen starvation and have low levels of amino acids. Remarkably, addition of glutamate or glutamine restores viability to a tor1 pep3 mutant strain. We conclude that Tor1 is more effective than Tor2 at providing rapamycin-sensitive Tor signaling under conditions of amino acid limitation, and that an intact class C Vps complex is required to mediate intracellular amino acid homeostasis for efficient Tor signaling.</div>
</front>
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<Abstract><AbstractText>The Tor kinases regulate responses to nutrients and control cell growth. Unlike most organisms that only contain one Tor protein, Saccharomyces cerevisiae expresses two, Tor1 and Tor2, which are thought to share all of the rapamycin-sensitive functions attributable to Tor signaling. Here we conducted a genetic screen that defined the global TOR1 synthetic fitness or lethal interaction gene network. This screen identified mutations in distinctive functional categories that impaired vacuolar function, including components of the EGO/Gse and PAS complexes that reduce fitness. In addition, tor1 is lethal in combination with mutations in class C Vps complex components. We find that Tor1 does not regulate the known function of the class C Vps complex in protein sorting. Instead class C vps mutants fail to recover from rapamycin-induced growth arrest or to survive nitrogen starvation and have low levels of amino acids. Remarkably, addition of glutamate or glutamine restores viability to a tor1 pep3 mutant strain. We conclude that Tor1 is more effective than Tor2 at providing rapamycin-sensitive Tor signaling under conditions of amino acid limitation, and that an intact class C Vps complex is required to mediate intracellular amino acid homeostasis for efficient Tor signaling.</AbstractText>
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<AffiliationInfo><Affiliation>Department of Molecular Genetics and Microbiology, Duke University Medical Center, Durham, NC 27710, USA.</Affiliation>
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<ForeName>Rekha</ForeName>
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Efficient Tor signaling requires a functional class C Vps protein complex in Saccharomyces cerevisiae.

Efficient Tor signaling requires a functional class C Vps protein complex in Saccharomyces cerevisiae.

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