RapamycinFungusV1, Main, Exploration, bibRecord, 001050

Five conditions commonly used to down-regulate tor complex 1 generate different physiological situations exhibiting distinct requirements and outcomes.

Identifieur interne : 001050 ( Main/Exploration ); précédent : 001049; suivant : 001051

Five conditions commonly used to down-regulate tor complex 1 generate different physiological situations exhibiting distinct requirements and outcomes.

Auteurs : Jennifer J. Tate [États-Unis] ; Terrance G. Cooper

Source :

The Journal of biological chemistry [ 1083-351X ] ; 2013.

RBID : pubmed:23935103

Descripteurs français

English descriptors

KwdEn :
- Antifungal Agents (pharmacology), Down-Regulation (drug effects), Down-Regulation (physiology), G1 Phase Cell Cycle Checkpoints (drug effects), G1 Phase Cell Cycle Checkpoints (physiology), Gene Expression Regulation, Fungal (drug effects), Gene Expression Regulation, Fungal (physiology), Mechanistic Target of Rapamycin Complex 1 (MeSH), Multiprotein Complexes (biosynthesis), Multiprotein Complexes (genetics), Protein Phosphatase 2 (genetics), Protein Phosphatase 2 (metabolism), Saccharomyces cerevisiae (genetics), Saccharomyces cerevisiae (metabolism), Saccharomyces cerevisiae Proteins (genetics), Saccharomyces cerevisiae Proteins (metabolism), Signal Transduction (drug effects), Signal Transduction (physiology), Sirolimus (pharmacology), TOR Serine-Threonine Kinases (biosynthesis), TOR Serine-Threonine Kinases (genetics), Transcription Factors (genetics), Transcription Factors (metabolism).
MESH :
- chemical , biosynthesis : Multiprotein Complexes, TOR Serine-Threonine Kinases.
- chemical , genetics : Multiprotein Complexes, Protein Phosphatase 2, Saccharomyces cerevisiae Proteins, TOR Serine-Threonine Kinases, Transcription Factors.
- chemical , metabolism : Protein Phosphatase 2, Saccharomyces cerevisiae Proteins, Transcription Factors.
- chemical , pharmacology : Antifungal Agents, Sirolimus.
- drug effects : Down-Regulation, G1 Phase Cell Cycle Checkpoints, Gene Expression Regulation, Fungal, Signal Transduction.
- genetics : Saccharomyces cerevisiae.
- metabolism : Saccharomyces cerevisiae.
- physiology : Down-Regulation, G1 Phase Cell Cycle Checkpoints, Gene Expression Regulation, Fungal, Signal Transduction.
- chemical : Mechanistic Target of Rapamycin Complex 1.

Abstract

Five different physiological conditions have been used interchangeably to establish the sequence of molecular events needed to achieve nitrogen-responsive down-regulation of TorC1 and its subsequent regulation of downstream reporters: nitrogen starvation, methionine sulfoximine (Msx) addition, nitrogen limitation, rapamycin addition, and leucine starvation. Therefore, we tested a specific underlying assumption upon which the interpretation of data generated by these five experimental perturbations is premised. It is that they generate physiologically equivalent outcomes with respect to TorC1, i.e. its down-regulation as reflected by TorC1 reporter responses. We tested this assumption by performing head-to-head comparisons of the requirements for each condition to achieve a common outcome for a downstream proxy of TorC1 inactivation, nuclear Gln3 localization. We demonstrate that the five conditions for down-regulating TorC1 do not elicit physiologically equivalent outcomes. Four of the methods exhibit hierarchical Sit4 and PP2A phosphatase requirements to elicit nuclear Gln3-Myc(13) localization. Rapamycin treatment required Sit4 and PP2A. Nitrogen limitation and short-term nitrogen starvation required only Sit4. G1 arrest-correlated, long-term nitrogen starvation and Msx treatment required neither PP2A nor Sit4. Starving cells of leucine or treating them with leucyl-tRNA synthetase inhibitors did not elicit nuclear Gln3-Myc(13) localization. These data indicate that the five commonly used nitrogen-related conditions of down-regulating TorC1 are not physiologically equivalent and minimally involve partially differing regulatory mechanisms. Further, identical requirements for Msx treatment and long-term nitrogen starvation raise the possibility that their effects are achieved through a common regulatory pathway with glutamine, a glutamate or glutamine metabolite level as the sensed metabolic signal.

DOI: 10.1074/jbc.M113.484386
PubMed: 23935103
PubMed Central: PMC3779721

Affiliations:

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

to stream Main, to step Corpus: 000F75
to stream Main, to step Curation: 000F75

Le document en format XML

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<term>G1 Phase Cell Cycle Checkpoints (drug effects)</term>
<term>G1 Phase Cell Cycle Checkpoints (physiology)</term>
<term>Gene Expression Regulation, Fungal (drug effects)</term>
<term>Gene Expression Regulation, Fungal (physiology)</term>
<term>Mechanistic Target of Rapamycin Complex 1 (MeSH)</term>
<term>Multiprotein Complexes (biosynthesis)</term>
<term>Multiprotein Complexes (genetics)</term>
<term>Protein Phosphatase 2 (genetics)</term>
<term>Protein Phosphatase 2 (metabolism)</term>
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<term>Saccharomyces cerevisiae (metabolism)</term>
<term>Saccharomyces cerevisiae Proteins (genetics)</term>
<term>Saccharomyces cerevisiae Proteins (metabolism)</term>
<term>Signal Transduction (drug effects)</term>
<term>Signal Transduction (physiology)</term>
<term>Sirolimus (pharmacology)</term>
<term>TOR Serine-Threonine Kinases (biosynthesis)</term>
<term>TOR Serine-Threonine Kinases (genetics)</term>
<term>Transcription Factors (genetics)</term>
<term>Transcription Factors (metabolism)</term>
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<keywords scheme="KwdFr" xml:lang="fr"><term>Antifongiques (pharmacologie)</term>
<term>Complexe-1 cible mécanistique de la rapamycine (MeSH)</term>
<term>Complexes multiprotéiques (biosynthèse)</term>
<term>Complexes multiprotéiques (génétique)</term>
<term>Facteurs de transcription (génétique)</term>
<term>Facteurs de transcription (métabolisme)</term>
<term>Points de contrôle de la phase G1 du cycle cellulaire (effets des médicaments et des substances chimiques)</term>
<term>Points de contrôle de la phase G1 du cycle cellulaire (physiologie)</term>
<term>Protein Phosphatase 2 (génétique)</term>
<term>Protein Phosphatase 2 (métabolisme)</term>
<term>Protéines de Saccharomyces cerevisiae (génétique)</term>
<term>Protéines de Saccharomyces cerevisiae (métabolisme)</term>
<term>Régulation de l'expression des gènes fongiques (effets des médicaments et des substances chimiques)</term>
<term>Régulation de l'expression des gènes fongiques (physiologie)</term>
<term>Régulation négative (effets des médicaments et des substances chimiques)</term>
<term>Régulation négative (physiologie)</term>
<term>Saccharomyces cerevisiae (génétique)</term>
<term>Saccharomyces cerevisiae (métabolisme)</term>
<term>Sirolimus (pharmacologie)</term>
<term>Sérine-thréonine kinases TOR (biosynthèse)</term>
<term>Sérine-thréonine kinases TOR (génétique)</term>
<term>Transduction du signal (effets des médicaments et des substances chimiques)</term>
<term>Transduction du signal (physiologie)</term>
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<term>TOR Serine-Threonine Kinases</term>
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<term>Protein Phosphatase 2</term>
<term>Saccharomyces cerevisiae Proteins</term>
<term>TOR Serine-Threonine Kinases</term>
<term>Transcription Factors</term>
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<term>Transcription Factors</term>
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<term>Gene Expression Regulation, Fungal</term>
<term>Signal Transduction</term>
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<term>Régulation de l'expression des gènes fongiques</term>
<term>Régulation négative</term>
<term>Transduction du signal</term>
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<term>Protéines de Saccharomyces cerevisiae</term>
<term>Saccharomyces cerevisiae</term>
<term>Sérine-thréonine kinases TOR</term>
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<term>Protéines de Saccharomyces cerevisiae</term>
<term>Saccharomyces cerevisiae</term>
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<term>Régulation de l'expression des gènes fongiques</term>
<term>Régulation négative</term>
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<front><div type="abstract" xml:lang="en">Five different physiological conditions have been used interchangeably to establish the sequence of molecular events needed to achieve nitrogen-responsive down-regulation of TorC1 and its subsequent regulation of downstream reporters: nitrogen starvation, methionine sulfoximine (Msx) addition, nitrogen limitation, rapamycin addition, and leucine starvation. Therefore, we tested a specific underlying assumption upon which the interpretation of data generated by these five experimental perturbations is premised. It is that they generate physiologically equivalent outcomes with respect to TorC1, i.e. its down-regulation as reflected by TorC1 reporter responses. We tested this assumption by performing head-to-head comparisons of the requirements for each condition to achieve a common outcome for a downstream proxy of TorC1 inactivation, nuclear Gln3 localization. We demonstrate that the five conditions for down-regulating TorC1 do not elicit physiologically equivalent outcomes. Four of the methods exhibit hierarchical Sit4 and PP2A phosphatase requirements to elicit nuclear Gln3-Myc(13) localization. Rapamycin treatment required Sit4 and PP2A. Nitrogen limitation and short-term nitrogen starvation required only Sit4. G1 arrest-correlated, long-term nitrogen starvation and Msx treatment required neither PP2A nor Sit4. Starving cells of leucine or treating them with leucyl-tRNA synthetase inhibitors did not elicit nuclear Gln3-Myc(13) localization. These data indicate that the five commonly used nitrogen-related conditions of down-regulating TorC1 are not physiologically equivalent and minimally involve partially differing regulatory mechanisms. Further, identical requirements for Msx treatment and long-term nitrogen starvation raise the possibility that their effects are achieved through a common regulatory pathway with glutamine, a glutamate or glutamine metabolite level as the sensed metabolic signal. </div>
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<ArticleTitle>Five conditions commonly used to down-regulate tor complex 1 generate different physiological situations exhibiting distinct requirements and outcomes.</ArticleTitle>
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<Abstract><AbstractText>Five different physiological conditions have been used interchangeably to establish the sequence of molecular events needed to achieve nitrogen-responsive down-regulation of TorC1 and its subsequent regulation of downstream reporters: nitrogen starvation, methionine sulfoximine (Msx) addition, nitrogen limitation, rapamycin addition, and leucine starvation. Therefore, we tested a specific underlying assumption upon which the interpretation of data generated by these five experimental perturbations is premised. It is that they generate physiologically equivalent outcomes with respect to TorC1, i.e. its down-regulation as reflected by TorC1 reporter responses. We tested this assumption by performing head-to-head comparisons of the requirements for each condition to achieve a common outcome for a downstream proxy of TorC1 inactivation, nuclear Gln3 localization. We demonstrate that the five conditions for down-regulating TorC1 do not elicit physiologically equivalent outcomes. Four of the methods exhibit hierarchical Sit4 and PP2A phosphatase requirements to elicit nuclear Gln3-Myc(13) localization. Rapamycin treatment required Sit4 and PP2A. Nitrogen limitation and short-term nitrogen starvation required only Sit4. G1 arrest-correlated, long-term nitrogen starvation and Msx treatment required neither PP2A nor Sit4. Starving cells of leucine or treating them with leucyl-tRNA synthetase inhibitors did not elicit nuclear Gln3-Myc(13) localization. These data indicate that the five commonly used nitrogen-related conditions of down-regulating TorC1 are not physiologically equivalent and minimally involve partially differing regulatory mechanisms. Further, identical requirements for Msx treatment and long-term nitrogen starvation raise the possibility that their effects are achieved through a common regulatory pathway with glutamine, a glutamate or glutamine metabolite level as the sensed metabolic signal. </AbstractText>
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<ForeName>Jennifer J</ForeName>
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<AffiliationInfo><Affiliation>From the Department of Microbiology, Immunology, and Biochemistry, University of Tennessee Health Science Center, Memphis, Tennessee 38163.</Affiliation>
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	Serveur d'exploration sur la rapamycine et les champignons
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Five conditions commonly used to down-regulate tor complex 1 generate different physiological situations exhibiting distinct requirements and outcomes.

Five conditions commonly used to down-regulate tor complex 1 generate different physiological situations exhibiting distinct requirements and outcomes.

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