Partitioning the transcriptional program induced by rapamycin among the effectors of the Tor proteins.
Identifieur interne : 001A25 ( Main/Exploration ); précédent : 001A24; suivant : 001A26Partitioning the transcriptional program induced by rapamycin among the effectors of the Tor proteins.
Auteurs : A F Shamji [États-Unis] ; F G Kuruvilla ; S L SchreiberSource :
- Current biology : CB [ 0960-9822 ]
Descripteurs français
- KwdFr :
- Analyse de profil d'expression de gènes (MeSH), Azote (métabolisme), Carbone (métabolisme), Phosphotransferases (Alcohol Group Acceptor) (génétique), Phosphotransferases (Alcohol Group Acceptor) (métabolisme), Protéines fongiques (génétique), Protéines fongiques (métabolisme), Régulation de l'expression des gènes fongiques (MeSH), Saccharomyces cerevisiae (effets des médicaments et des substances chimiques), Saccharomyces cerevisiae (génétique), Saccharomyces cerevisiae (physiologie), Sirolimus (pharmacologie), Transcription génétique (MeSH), Transduction du signal (physiologie).
- MESH :
- effets des médicaments et des substances chimiques : Saccharomyces cerevisiae.
- génétique : Phosphotransferases (Alcohol Group Acceptor), Protéines fongiques, Saccharomyces cerevisiae.
- métabolisme : Azote, Carbone, Phosphotransferases (Alcohol Group Acceptor), Protéines fongiques.
- pharmacologie : Sirolimus.
- physiologie : Saccharomyces cerevisiae, Transduction du signal.
- Analyse de profil d'expression de gènes, Régulation de l'expression des gènes fongiques, Transcription génétique.
English descriptors
- KwdEn :
- Carbon (metabolism), Fungal Proteins (genetics), Fungal Proteins (metabolism), Gene Expression Profiling (MeSH), Gene Expression Regulation, Fungal (MeSH), Nitrogen (metabolism), Phosphotransferases (Alcohol Group Acceptor) (genetics), Phosphotransferases (Alcohol Group Acceptor) (metabolism), Saccharomyces cerevisiae (drug effects), Saccharomyces cerevisiae (genetics), Saccharomyces cerevisiae (physiology), Signal Transduction (physiology), Sirolimus (pharmacology), Transcription, Genetic (MeSH).
- MESH :
- chemical , genetics : Fungal Proteins, Phosphotransferases (Alcohol Group Acceptor).
- chemical , metabolism : Carbon, Fungal Proteins, Nitrogen, Phosphotransferases (Alcohol Group Acceptor).
- drug effects : Saccharomyces cerevisiae.
- genetics : Saccharomyces cerevisiae.
- chemical , pharmacology : Sirolimus.
- physiology : Saccharomyces cerevisiae, Signal Transduction.
- Gene Expression Profiling, Gene Expression Regulation, Fungal, Transcription, Genetic.
Abstract
BACKGROUND
In all organisms, nutrients are primary regulators of signaling pathways that control transcription. In Saccharomyces cerevisiae, the Tor proteins regulate the transcription of genes sensitive to the quality of available nitrogen and carbon sources. Formation of a ternary complex of the immunosuppressant rapamycin, its immunophilin receptor Fpr1p and Tor1p or Tor2p results in the nuclear import of several nutrient- and stress-responsive transcription factors.
RESULTS
We show that treating yeast cells with rapamycin results in a broader modulation of functionally related gene sets than previously understood. Using chemical epistasis and vector-based global expression analyses, we partition the transcriptional program induced by rapamycin among five effectors (TAP42, MKS1, URE2, GLN3, GAT1) of the Tor proteins, and identify how the quality of carbon and nitrogen sources impinge upon components of the program. Biochemical data measuring Ure2p phosphorylation coupled with the partition analysis indicate that there are distinct signaling branches downstream of the Tor proteins.
CONCLUSIONS
Whole-genome transcription profiling reveals a striking similarity between shifting to low-quality carbon or nitrogen sources and treatment with rapamycin. These data suggest that the Tor proteins are central sensors of the quality of carbon and nitrogen sources. Depending on which nutrient is limited in quality, the Tor proteins can modulate a given pathway differentially. Integrating the partition analysis of the transcriptional program of rapamycin with the biochemical data, we propose a novel architecture of Tor protein signaling and of the nutrient-response network, including the identification of carbon discrimination and nitrogen discrimination pathways.
DOI: 10.1016/s0960-9822(00)00866-6
PubMed: 11137008
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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type="state">Massachusetts</region></placeName></affiliation></author><author><name sortKey="Kuruvilla, F G" sort="Kuruvilla, F G" uniqKey="Kuruvilla F" first="F G" last="Kuruvilla">F G Kuruvilla</name></author><author><name sortKey="Schreiber, S L" sort="Schreiber, S L" uniqKey="Schreiber S" first="S L" last="Schreiber">S L Schreiber</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2000">2000 Dec 14-28</date><idno type="RBID">pubmed:11137008</idno><idno type="pmid">11137008</idno><idno type="doi">10.1016/s0960-9822(00)00866-6</idno><idno type="wicri:Area/Main/Corpus">001A23</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Corpus" wicri:corpus="PubMed">001A23</idno><idno type="wicri:Area/Main/Curation">001A23</idno><idno type="wicri:explorRef" wicri:stream="Main" wicri:step="Curation">001A23</idno><idno type="wicri:Area/Main/Exploration">001A23</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Partitioning the transcriptional program induced by rapamycin among the effectors of the Tor proteins.</title><author><name sortKey="Shamji, A F" sort="Shamji, A F" uniqKey="Shamji A" first="A F" last="Shamji">A F Shamji</name><affiliation wicri:level="4"><nlm:affiliation>Howard Hughes Medical Institute, Center for Genomics Research, Department of Chemistry and Chemical Biology, Harvard University, 12 Oxford Street, Cambridge, Massachusetts 02138, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Howard Hughes Medical Institute, Center for Genomics Research, Department of Chemistry and Chemical Biology, Harvard University, 12 Oxford Street, Cambridge, Massachusetts 02138</wicri:regionArea><orgName type="university">Université Harvard</orgName><placeName><settlement type="city">Cambridge (Massachusetts)</settlement><region type="state">Massachusetts</region></placeName></affiliation></author><author><name sortKey="Kuruvilla, F G" sort="Kuruvilla, F G" uniqKey="Kuruvilla F" first="F G" last="Kuruvilla">F G Kuruvilla</name></author><author><name sortKey="Schreiber, S L" sort="Schreiber, S L" uniqKey="Schreiber S" first="S L" last="Schreiber">S L Schreiber</name></author></analytic><series><title level="j">Current biology : CB</title><idno type="ISSN">0960-9822</idno></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Carbon (metabolism)</term><term>Fungal Proteins (genetics)</term><term>Fungal Proteins (metabolism)</term><term>Gene Expression Profiling (MeSH)</term><term>Gene Expression Regulation, Fungal (MeSH)</term><term>Nitrogen (metabolism)</term><term>Phosphotransferases (Alcohol Group Acceptor) (genetics)</term><term>Phosphotransferases (Alcohol Group Acceptor) (metabolism)</term><term>Saccharomyces cerevisiae (drug effects)</term><term>Saccharomyces cerevisiae (genetics)</term><term>Saccharomyces cerevisiae (physiology)</term><term>Signal 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Proteins</term><term>Phosphotransferases (Alcohol Group Acceptor)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Carbon</term><term>Fungal Proteins</term><term>Nitrogen</term><term>Phosphotransferases (Alcohol Group Acceptor)</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Saccharomyces cerevisiae</term></keywords><keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Saccharomyces cerevisiae</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Saccharomyces cerevisiae</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Phosphotransferases (Alcohol Group Acceptor)</term><term>Protéines fongiques</term><term>Saccharomyces cerevisiae</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Azote</term><term>Carbone</term><term>Phosphotransferases (Alcohol Group Acceptor)</term><term>Protéines fongiques</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Sirolimus</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Sirolimus</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Saccharomyces cerevisiae</term><term>Transduction du signal</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Saccharomyces cerevisiae</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Gene Expression Profiling</term><term>Gene Expression Regulation, Fungal</term><term>Transcription, Genetic</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Analyse de profil d'expression de gènes</term><term>Régulation de l'expression des gènes fongiques</term><term>Transcription génétique</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p><b>BACKGROUND</b></p><p>In all organisms, nutrients are primary regulators of signaling pathways that control transcription. In Saccharomyces cerevisiae, the Tor proteins regulate the transcription of genes sensitive to the quality of available nitrogen and carbon sources. Formation of a ternary complex of the immunosuppressant rapamycin, its immunophilin receptor Fpr1p and Tor1p or Tor2p results in the nuclear import of several nutrient- and stress-responsive transcription factors.</p></div><div type="abstract" xml:lang="en"><p><b>RESULTS</b></p><p>We show that treating yeast cells with rapamycin results in a broader modulation of functionally related gene sets than previously understood. Using chemical epistasis and vector-based global expression analyses, we partition the transcriptional program induced by rapamycin among five effectors (TAP42, MKS1, URE2, GLN3, GAT1) of the Tor proteins, and identify how the quality of carbon and nitrogen sources impinge upon components of the program. Biochemical data measuring Ure2p phosphorylation coupled with the partition analysis indicate that there are distinct signaling branches downstream of the Tor proteins.</p></div><div type="abstract" xml:lang="en"><p><b>CONCLUSIONS</b></p><p>Whole-genome transcription profiling reveals a striking similarity between shifting to low-quality carbon or nitrogen sources and treatment with rapamycin. These data suggest that the Tor proteins are central sensors of the quality of carbon and nitrogen sources. Depending on which nutrient is limited in quality, the Tor proteins can modulate a given pathway differentially. Integrating the partition analysis of the transcriptional program of rapamycin with the biochemical data, we propose a novel architecture of Tor protein signaling and of the nutrient-response network, including the identification of carbon discrimination and nitrogen discrimination pathways.</p></div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">11137008</PMID><DateCompleted><Year>2001</Year><Month>06</Month><Day>14</Day></DateCompleted><DateRevised><Year>2019</Year><Month>07</Month><Day>28</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0960-9822</ISSN><JournalIssue CitedMedium="Print"><Volume>10</Volume><Issue>24</Issue><PubDate><MedlineDate>2000 Dec 14-28</MedlineDate></PubDate></JournalIssue><Title>Current biology : CB</Title><ISOAbbreviation>Curr Biol</ISOAbbreviation></Journal><ArticleTitle>Partitioning the transcriptional program induced by rapamycin among the effectors of the Tor proteins.</ArticleTitle><Pagination><MedlinePgn>1574-81</MedlinePgn></Pagination><Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">In all organisms, nutrients are primary regulators of signaling pathways that control transcription. In Saccharomyces cerevisiae, the Tor proteins regulate the transcription of genes sensitive to the quality of available nitrogen and carbon sources. Formation of a ternary complex of the immunosuppressant rapamycin, its immunophilin receptor Fpr1p and Tor1p or Tor2p results in the nuclear import of several nutrient- and stress-responsive transcription factors.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">We show that treating yeast cells with rapamycin results in a broader modulation of functionally related gene sets than previously understood. Using chemical epistasis and vector-based global expression analyses, we partition the transcriptional program induced by rapamycin among five effectors (TAP42, MKS1, URE2, GLN3, GAT1) of the Tor proteins, and identify how the quality of carbon and nitrogen sources impinge upon components of the program. Biochemical data measuring Ure2p phosphorylation coupled with the partition analysis indicate that there are distinct signaling branches downstream of the Tor proteins.</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">Whole-genome transcription profiling reveals a striking similarity between shifting to low-quality carbon or nitrogen sources and treatment with rapamycin. These data suggest that the Tor proteins are central sensors of the quality of carbon and nitrogen sources. Depending on which nutrient is limited in quality, the Tor proteins can modulate a given pathway differentially. Integrating the partition analysis of the transcriptional program of rapamycin with the biochemical data, we propose a novel architecture of Tor protein signaling and of the nutrient-response network, including the identification of carbon discrimination and nitrogen discrimination pathways.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Shamji</LastName><ForeName>A F</ForeName><Initials>AF</Initials><AffiliationInfo><Affiliation>Howard Hughes Medical Institute, Center for Genomics Research, Department of Chemistry and Chemical Biology, Harvard University, 12 Oxford Street, Cambridge, Massachusetts 02138, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kuruvilla</LastName><ForeName>F G</ForeName><Initials>FG</Initials></Author><Author ValidYN="Y"><LastName>Schreiber</LastName><ForeName>S L</ForeName><Initials>SL</Initials></Author></AuthorList><Language>eng</Language><GrantList 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MajorTopicYN="N">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020123" MajorTopicYN="N">Sirolimus</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014158" MajorTopicYN="Y">Transcription, Genetic</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2001</Year><Month>1</Month><Day>4</Day><Hour>11</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2001</Year><Month>6</Month><Day>23</Day><Hour>10</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2001</Year><Month>1</Month><Day>4</Day><Hour>11</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">11137008</ArticleId><ArticleId IdType="pii">S0960-9822(00)00866-6</ArticleId><ArticleId IdType="doi">10.1016/s0960-9822(00)00866-6</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>États-Unis</li></country><region><li>Massachusetts</li></region><settlement><li>Cambridge (Massachusetts)</li></settlement><orgName><li>Université Harvard</li></orgName></list><tree><noCountry><name sortKey="Kuruvilla, F G" sort="Kuruvilla, F G" uniqKey="Kuruvilla F" first="F G" last="Kuruvilla">F G Kuruvilla</name><name sortKey="Schreiber, S L" sort="Schreiber, S L" uniqKey="Schreiber S" first="S L" last="Schreiber">S L Schreiber</name></noCountry><country name="États-Unis"><region name="Massachusetts"><name sortKey="Shamji, A F" sort="Shamji, A F" uniqKey="Shamji A" first="A F" last="Shamji">A F Shamji</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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