RapamycinFungusV1, Main, Exploration, bibRecord, 000709

The nutrient transceptor/PKA pathway functions independently of TOR and responds to leucine and Gcn2 in a TOR-independent manner.

Identifieur interne : 000709 ( Main/Exploration ); précédent : 000708; suivant : 000710

The nutrient transceptor/PKA pathway functions independently of TOR and responds to leucine and Gcn2 in a TOR-independent manner.

Auteurs : Michaela Conrad [Belgique] ; Harish Nag Kankipati [Belgique] ; Marlies Kimpe [Belgique] ; Griet Van Zeebroeck [Belgique] ; Zhiqiang Zhang [Belgique] ; Johan M. Thevelein [Belgique]

Source :

FEMS yeast research [ 1567-1364 ] ; 2017.

RBID : pubmed:28810702

Descripteurs français

English descriptors

KwdEn :
- Amino Acid Transport Systems (metabolism), Cyclic AMP-Dependent Protein Kinases (metabolism), Leucine (metabolism), Phosphorylation (MeSH), Protein Processing, Post-Translational (MeSH), Protein-Serine-Threonine Kinases (metabolism), Proton-Phosphate Symporters (metabolism), Saccharomyces cerevisiae (enzymology), Saccharomyces cerevisiae (metabolism), Saccharomyces cerevisiae Proteins (metabolism), Signal Transduction (MeSH), Transcription Factors (metabolism).
MESH :
- chemical , metabolism : Amino Acid Transport Systems, Cyclic AMP-Dependent Protein Kinases, Leucine, Protein-Serine-Threonine Kinases, Proton-Phosphate Symporters, Saccharomyces cerevisiae Proteins, Transcription Factors.
- enzymology : Saccharomyces cerevisiae.
- metabolism : Saccharomyces cerevisiae.
- Phosphorylation, Protein Processing, Post-Translational, Signal Transduction.

Abstract

Two nutrient-controlled signalling pathways, the PKA and TOR pathway, play a major role in nutrient regulation of growth as well as growth-correlated properties in yeast. The relationship between the two pathways is not well understood. We have used Gap1 and Pho84 transceptor-mediated activation of trehalase and phosphorylation of fragmented Sch9 as a read-out for rapid nutrient activation of PKA or TORC1, respectively. We have identified conditions in which L-citrulline-induced activation of Sch9 phosphorylation is compromised, but not activation of trehalase: addition of the TORC1 inhibitor, rapamycin and low levels of L-citrulline. The same disconnection was observed for phosphate activation in phosphate-starved cells. The leu2 auxotrophic mutation reduces amino acid activation of trehalase, which is counteracted by deletion of GCN2. Both effects were also independent of TORC1. Our results show that rapid activation of the TOR pathway by amino acids is not involved in rapid activation of the PKA pathway and that effects of Gcn2 inactivation as well as leu2 auxotrophy all act independently of the TOR pathway. Hence, rapid nutrient signalling to PKA and TOR in cells arrested by nutrient starvation acts through parallel pathways.

DOI: 10.1093/femsyr/fox048
PubMed: 28810702
PubMed Central: PMC5812495

Affiliations:

Belgique

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Le document en format XML

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<term>Cyclic AMP-Dependent Protein Kinases (metabolism)</term>
<term>Leucine (metabolism)</term>
<term>Phosphorylation (MeSH)</term>
<term>Protein Processing, Post-Translational (MeSH)</term>
<term>Protein-Serine-Threonine Kinases (metabolism)</term>
<term>Proton-Phosphate Symporters (metabolism)</term>
<term>Saccharomyces cerevisiae (enzymology)</term>
<term>Saccharomyces cerevisiae (metabolism)</term>
<term>Saccharomyces cerevisiae Proteins (metabolism)</term>
<term>Signal Transduction (MeSH)</term>
<term>Transcription Factors (metabolism)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Cyclic AMP-Dependent Protein Kinases (métabolisme)</term>
<term>Facteurs de transcription (métabolisme)</term>
<term>Leucine (métabolisme)</term>
<term>Maturation post-traductionnelle des protéines (MeSH)</term>
<term>Phosphorylation (MeSH)</term>
<term>Protein-Serine-Threonine Kinases (métabolisme)</term>
<term>Protéines de Saccharomyces cerevisiae (métabolisme)</term>
<term>Saccharomyces cerevisiae (enzymologie)</term>
<term>Saccharomyces cerevisiae (métabolisme)</term>
<term>Symporteurs des ions proton-phosphate (métabolisme)</term>
<term>Systèmes de transport d'acides aminés (métabolisme)</term>
<term>Transduction du signal (MeSH)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Amino Acid Transport Systems</term>
<term>Cyclic AMP-Dependent Protein Kinases</term>
<term>Leucine</term>
<term>Protein-Serine-Threonine Kinases</term>
<term>Proton-Phosphate Symporters</term>
<term>Saccharomyces cerevisiae Proteins</term>
<term>Transcription Factors</term>
</keywords>
<keywords scheme="MESH" qualifier="enzymologie" xml:lang="fr"><term>Saccharomyces cerevisiae</term>
</keywords>
<keywords scheme="MESH" qualifier="enzymology" xml:lang="en"><term>Saccharomyces cerevisiae</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Saccharomyces cerevisiae</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Cyclic AMP-Dependent Protein Kinases</term>
<term>Facteurs de transcription</term>
<term>Leucine</term>
<term>Protein-Serine-Threonine Kinases</term>
<term>Protéines de Saccharomyces cerevisiae</term>
<term>Saccharomyces cerevisiae</term>
<term>Symporteurs des ions proton-phosphate</term>
<term>Systèmes de transport d'acides aminés</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Phosphorylation</term>
<term>Protein Processing, Post-Translational</term>
<term>Signal Transduction</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Maturation post-traductionnelle des protéines</term>
<term>Phosphorylation</term>
<term>Transduction du signal</term>
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<front><div type="abstract" xml:lang="en">Two nutrient-controlled signalling pathways, the PKA and TOR pathway, play a major role in nutrient regulation of growth as well as growth-correlated properties in yeast. The relationship between the two pathways is not well understood. We have used Gap1 and Pho84 transceptor-mediated activation of trehalase and phosphorylation of fragmented Sch9 as a read-out for rapid nutrient activation of PKA or TORC1, respectively. We have identified conditions in which L-citrulline-induced activation of Sch9 phosphorylation is compromised, but not activation of trehalase: addition of the TORC1 inhibitor, rapamycin and low levels of L-citrulline. The same disconnection was observed for phosphate activation in phosphate-starved cells. The leu2 auxotrophic mutation reduces amino acid activation of trehalase, which is counteracted by deletion of GCN2. Both effects were also independent of TORC1. Our results show that rapid activation of the TOR pathway by amino acids is not involved in rapid activation of the PKA pathway and that effects of Gcn2 inactivation as well as leu2 auxotrophy all act independently of the TOR pathway. Hence, rapid nutrient signalling to PKA and TOR in cells arrested by nutrient starvation acts through parallel pathways.</div>
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<DateCompleted><Year>2018</Year>
<Month>04</Month>
<Day>30</Day>
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<DateRevised><Year>2018</Year>
<Month>11</Month>
<Day>13</Day>
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<Month>08</Month>
<Day>01</Day>
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<Title>FEMS yeast research</Title>
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<ArticleTitle>The nutrient transceptor/PKA pathway functions independently of TOR and responds to leucine and Gcn2 in a TOR-independent manner.</ArticleTitle>
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<Abstract><AbstractText>Two nutrient-controlled signalling pathways, the PKA and TOR pathway, play a major role in nutrient regulation of growth as well as growth-correlated properties in yeast. The relationship between the two pathways is not well understood. We have used Gap1 and Pho84 transceptor-mediated activation of trehalase and phosphorylation of fragmented Sch9 as a read-out for rapid nutrient activation of PKA or TORC1, respectively. We have identified conditions in which L-citrulline-induced activation of Sch9 phosphorylation is compromised, but not activation of trehalase: addition of the TORC1 inhibitor, rapamycin and low levels of L-citrulline. The same disconnection was observed for phosphate activation in phosphate-starved cells. The leu2 auxotrophic mutation reduces amino acid activation of trehalase, which is counteracted by deletion of GCN2. Both effects were also independent of TORC1. Our results show that rapid activation of the TOR pathway by amino acids is not involved in rapid activation of the PKA pathway and that effects of Gcn2 inactivation as well as leu2 auxotrophy all act independently of the TOR pathway. Hence, rapid nutrient signalling to PKA and TOR in cells arrested by nutrient starvation acts through parallel pathways.</AbstractText>
<CopyrightInformation>© FEMS 2017.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Conrad</LastName>
<ForeName>Michaela</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Laboratory of Molecular Cell Biology, Institute of Botany and Microbiology, B-3001 KU Leuven, Belgium.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Center for Microbiology, VIB, Kasteelpark Arenberg 31, B-3001 Leuven-Heverlee, Flanders, Belgium.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Kankipati</LastName>
<ForeName>Harish Nag</ForeName>
<Initials>HN</Initials>
<AffiliationInfo><Affiliation>Laboratory of Molecular Cell Biology, Institute of Botany and Microbiology, B-3001 KU Leuven, Belgium.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Center for Microbiology, VIB, Kasteelpark Arenberg 31, B-3001 Leuven-Heverlee, Flanders, Belgium.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Kimpe</LastName>
<ForeName>Marlies</ForeName>
<Initials>M</Initials>
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</AffiliationInfo>
<AffiliationInfo><Affiliation>Center for Microbiology, VIB, Kasteelpark Arenberg 31, B-3001 Leuven-Heverlee, Flanders, Belgium.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Van Zeebroeck</LastName>
<ForeName>Griet</ForeName>
<Initials>G</Initials>
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</AffiliationInfo>
<AffiliationInfo><Affiliation>Center for Microbiology, VIB, Kasteelpark Arenberg 31, B-3001 Leuven-Heverlee, Flanders, Belgium.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Zhang</LastName>
<ForeName>Zhiqiang</ForeName>
<Initials>Z</Initials>
<AffiliationInfo><Affiliation>Laboratory of Molecular Cell Biology, Institute of Botany and Microbiology, B-3001 KU Leuven, Belgium.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Center for Microbiology, VIB, Kasteelpark Arenberg 31, B-3001 Leuven-Heverlee, Flanders, Belgium.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Thevelein</LastName>
<ForeName>Johan M</ForeName>
<Initials>JM</Initials>
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	Serveur d'exploration sur la rapamycine et les champignons
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The nutrient transceptor/PKA pathway functions independently of TOR and responds to leucine and Gcn2 in a TOR-independent manner.

The nutrient transceptor/PKA pathway functions independently of TOR and responds to leucine and Gcn2 in a TOR-independent manner.

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