RapamycinFungusV1, Main, Exploration, bibRecord, 001A53

Rapamycin-modulated transcription defines the subset of nutrient-sensitive signaling pathways directly controlled by the Tor proteins.

Identifieur interne : 001A53 ( Main/Exploration ); précédent : 001A52; suivant : 001A54

Rapamycin-modulated transcription defines the subset of nutrient-sensitive signaling pathways directly controlled by the Tor proteins.

Auteurs : J S Hardwick [États-Unis] ; F G Kuruvilla ; J K Tong ; A F Shamji ; S L Schreiber

Source :

Proceedings of the National Academy of Sciences of the United States of America [ 0027-8424 ] ; 1999.

RBID : pubmed:10611304

Descripteurs français

KwdFr :
- Analyse de profil d'expression de gènes (MeSH), Azote (métabolisme), Cycle citrique (physiologie), Glucose (métabolisme), Glutathione peroxidase (MeSH), Glycolyse (physiologie), Hybridation d'acides nucléiques (MeSH), Milieux de culture (MeSH), Phosphatidylinositol 3-kinases (MeSH), Phosphotransferases (Alcohol Group Acceptor) (métabolisme), Prions (MeSH), Protéines de Saccharomyces cerevisiae (MeSH), Protéines de répression (métabolisme), Protéines du cycle cellulaire (MeSH), Protéines fongiques (métabolisme), Saccharomyces cerevisiae (physiologie), Sirolimus (pharmacologie), Séquençage par oligonucléotides en batterie (MeSH), Transcription génétique (effets des médicaments et des substances chimiques), Transduction du signal (MeSH).
MESH :
- effets des médicaments et des substances chimiques : Transcription génétique.
- métabolisme : Azote, Glucose, Phosphotransferases (Alcohol Group Acceptor), Protéines de répression, Protéines fongiques.
- pharmacologie : Sirolimus.
- physiologie : Cycle citrique, Glycolyse, Saccharomyces cerevisiae.
- Analyse de profil d'expression de gènes, Glutathione peroxidase, Hybridation d'acides nucléiques, Milieux de culture, Phosphatidylinositol 3-kinases, Prions, Protéines de Saccharomyces cerevisiae, Protéines du cycle cellulaire, Séquençage par oligonucléotides en batterie, Transduction du signal.

English descriptors

KwdEn :
- Cell Cycle Proteins (MeSH), Citric Acid Cycle (physiology), Culture Media (MeSH), Fungal Proteins (metabolism), Gene Expression Profiling (MeSH), Glucose (metabolism), Glutathione Peroxidase (MeSH), Glycolysis (physiology), Nitrogen (metabolism), Nucleic Acid Hybridization (MeSH), Oligonucleotide Array Sequence Analysis (MeSH), Phosphatidylinositol 3-Kinases (MeSH), Phosphotransferases (Alcohol Group Acceptor) (metabolism), Prions (MeSH), Repressor Proteins (metabolism), Saccharomyces cerevisiae (physiology), Saccharomyces cerevisiae Proteins (MeSH), Signal Transduction (MeSH), Sirolimus (pharmacology), Transcription, Genetic (drug effects).
MESH :
- chemical , metabolism : Fungal Proteins, Glucose, Nitrogen, Phosphotransferases (Alcohol Group Acceptor), Repressor Proteins.
- chemical , pharmacology : Sirolimus.
- chemical : Cell Cycle Proteins, Culture Media, Glutathione Peroxidase, Phosphatidylinositol 3-Kinases, Prions, Saccharomyces cerevisiae Proteins.
- drug effects : Transcription, Genetic.
- physiology : Citric Acid Cycle, Glycolysis, Saccharomyces cerevisiae.
- Gene Expression Profiling, Nucleic Acid Hybridization, Oligonucleotide Array Sequence Analysis, Signal Transduction.

Abstract

The immunosuppressant rapamycin inhibits Tor1p and Tor2p (target of rapamycin proteins), ultimately resulting in cellular responses characteristic of nutrient deprivation through a mechanism involving translational arrest. We measured the immediate transcriptional response of yeast grown in rich media and treated with rapamycin to investigate the direct effects of Tor proteins on nutrient-sensitive signaling pathways. The results suggest that Tor proteins directly modulate the glucose activation and nitrogen discrimination pathways and the pathways that respond to the diauxic shift (including glycolysis and the citric acid cycle). Tor proteins do not directly modulate the general amino acid control, nitrogen starvation, or sporulation (in diploid cells) pathways. Poor nitrogen quality activates the nitrogen discrimination pathway, which is controlled by the complex of the transcriptional repressor Ure2p and activator Gln3p. Inhibiting Tor proteins with rapamycin increases the electrophoretic mobility of Ure2p. The work presented here illustrates the coordinated use of genome-based and biochemical approaches to delineate a cellular pathway modulated by the protein target of a small molecule.

DOI: 10.1073/pnas.96.26.14866
PubMed: 10611304
PubMed Central: PMC24739

Affiliations:

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Le document en format XML

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<front><div type="abstract" xml:lang="en">The immunosuppressant rapamycin inhibits Tor1p and Tor2p (target of rapamycin proteins), ultimately resulting in cellular responses characteristic of nutrient deprivation through a mechanism involving translational arrest. We measured the immediate transcriptional response of yeast grown in rich media and treated with rapamycin to investigate the direct effects of Tor proteins on nutrient-sensitive signaling pathways. The results suggest that Tor proteins directly modulate the glucose activation and nitrogen discrimination pathways and the pathways that respond to the diauxic shift (including glycolysis and the citric acid cycle). Tor proteins do not directly modulate the general amino acid control, nitrogen starvation, or sporulation (in diploid cells) pathways. Poor nitrogen quality activates the nitrogen discrimination pathway, which is controlled by the complex of the transcriptional repressor Ure2p and activator Gln3p. Inhibiting Tor proteins with rapamycin increases the electrophoretic mobility of Ure2p. The work presented here illustrates the coordinated use of genome-based and biochemical approaches to delineate a cellular pathway modulated by the protein target of a small molecule.</div>
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Rapamycin-modulated transcription defines the subset of nutrient-sensitive signaling pathways directly controlled by the Tor proteins.

Rapamycin-modulated transcription defines the subset of nutrient-sensitive signaling pathways directly controlled by the Tor proteins.

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