RapamycinFungusV1, Main, Exploration, bibRecord, 001503

Nitrogen catabolite repression-sensitive transcription as a readout of Tor pathway regulation: the genetic background, reporter gene and GATA factor assayed determine the outcomes.

Identifieur interne : 001503 ( Main/Exploration ); précédent : 001502; suivant : 001504

Nitrogen catabolite repression-sensitive transcription as a readout of Tor pathway regulation: the genetic background, reporter gene and GATA factor assayed determine the outcomes.

Auteurs : Isabelle Georis [Belgique] ; André Feller ; Jennifer J. Tate ; Terrance G. Cooper ; Evelyne Dubois

Source :

Genetics [ 0016-6731 ] ; 2009.

RBID : pubmed:19104072

Descripteurs français

English descriptors

KwdEn :
- Down-Regulation (drug effects), GATA Transcription Factors (genetics), GATA Transcription Factors (metabolism), Gene Expression Regulation, Fungal (MeSH), Genes, Reporter (MeSH), Membrane Transport Proteins (genetics), Membrane Transport Proteins (metabolism), Nitrogen (metabolism), Protein Phosphatase 2 (genetics), Protein Phosphatase 2 (metabolism), Protein-Serine-Threonine Kinases (metabolism), Reproducibility of Results (MeSH), Saccharomyces cerevisiae (drug effects), Saccharomyces cerevisiae (genetics), Saccharomyces cerevisiae Proteins (genetics), Saccharomyces cerevisiae Proteins (metabolism), Signal Transduction (MeSH), Sirolimus (pharmacology), Transcription Factors (genetics), Transcription Factors (metabolism), Transcription, Genetic (drug effects).
MESH :
- chemical , genetics : GATA Transcription Factors, Membrane Transport Proteins, Protein Phosphatase 2, Saccharomyces cerevisiae Proteins, Transcription Factors.
- drug effects : Down-Regulation, Saccharomyces cerevisiae, Transcription, Genetic.
- genetics : Saccharomyces cerevisiae.
- chemical , metabolism : GATA Transcription Factors, Membrane Transport Proteins, Nitrogen, Protein Phosphatase 2, Protein-Serine-Threonine Kinases, Saccharomyces cerevisiae Proteins, Transcription Factors.
- chemical , pharmacology : Sirolimus.
- Gene Expression Regulation, Fungal, Genes, Reporter, Reproducibility of Results, Signal Transduction.

Abstract

Nitrogen catabolite repression (NCR)-sensitive genes, whose expression is highly repressed when provided with excess nitrogen and derepressed when nitrogen is limited or cells are treated with rapamycin, are routinely used as reporters in mechanistic studies of the Tor signal transduction pathway in Saccharomyces cerevisiae. Two GATA factors, Gln3 and Gat1, are responsible for NCR-sensitive transcription, but recent evidence demonstrates that Tor pathway regulation of NCR-sensitive transcription bifurcates at the level of GATA factor localization. Gln3 requires Sit4 phosphatase for nuclear localization and NCR-sensitive transcription while Gat1 does not. In this article, we demonstrate that the extent to which Sit4 plays a role in NCR-sensitive transcription depends upon whether or not (i) Gzf3, a GATA repressor homologous to Dal80, is active in the genetic background assayed; (ii) Gat1 is able to activate transcription of the assayed gene in the absence of Gln3 in that genetic background; and (iii) the gene chosen as a reporter is able to be transcribed by Gln3 or Gat1 in the absence of the other GATA factor. Together, the data indicate that in the absence of these three pieces of information, overall NCR-sensitive gene transcription data are unreliable as Tor pathway readouts.

DOI: 10.1534/genetics.108.099051
PubMed: 19104072
PubMed Central: PMC2651060

Affiliations:

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

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Le document en format XML

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<term>GATA Transcription Factors (genetics)</term>
<term>GATA Transcription Factors (metabolism)</term>
<term>Gene Expression Regulation, Fungal (MeSH)</term>
<term>Genes, Reporter (MeSH)</term>
<term>Membrane Transport Proteins (genetics)</term>
<term>Membrane Transport Proteins (metabolism)</term>
<term>Nitrogen (metabolism)</term>
<term>Protein Phosphatase 2 (genetics)</term>
<term>Protein Phosphatase 2 (metabolism)</term>
<term>Protein-Serine-Threonine Kinases (metabolism)</term>
<term>Reproducibility of Results (MeSH)</term>
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<term>Saccharomyces cerevisiae (genetics)</term>
<term>Saccharomyces cerevisiae Proteins (genetics)</term>
<term>Saccharomyces cerevisiae Proteins (metabolism)</term>
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<term>Sirolimus (pharmacology)</term>
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<term>Transcription Factors (metabolism)</term>
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<term>Protein Phosphatase 2 (métabolisme)</term>
<term>Protein-Serine-Threonine Kinases (métabolisme)</term>
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<term>Protéines de Saccharomyces cerevisiae (métabolisme)</term>
<term>Protéines de transport membranaire (génétique)</term>
<term>Protéines de transport membranaire (métabolisme)</term>
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<term>Régulation de l'expression des gènes fongiques (MeSH)</term>
<term>Régulation négative (effets des médicaments et des substances chimiques)</term>
<term>Saccharomyces cerevisiae (effets des médicaments et des substances chimiques)</term>
<term>Saccharomyces cerevisiae (génétique)</term>
<term>Sirolimus (pharmacologie)</term>
<term>Transcription génétique (effets des médicaments et des substances chimiques)</term>
<term>Transduction du signal (MeSH)</term>
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<term>Protein Phosphatase 2</term>
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<front><div type="abstract" xml:lang="en">Nitrogen catabolite repression (NCR)-sensitive genes, whose expression is highly repressed when provided with excess nitrogen and derepressed when nitrogen is limited or cells are treated with rapamycin, are routinely used as reporters in mechanistic studies of the Tor signal transduction pathway in Saccharomyces cerevisiae. Two GATA factors, Gln3 and Gat1, are responsible for NCR-sensitive transcription, but recent evidence demonstrates that Tor pathway regulation of NCR-sensitive transcription bifurcates at the level of GATA factor localization. Gln3 requires Sit4 phosphatase for nuclear localization and NCR-sensitive transcription while Gat1 does not. In this article, we demonstrate that the extent to which Sit4 plays a role in NCR-sensitive transcription depends upon whether or not (i) Gzf3, a GATA repressor homologous to Dal80, is active in the genetic background assayed; (ii) Gat1 is able to activate transcription of the assayed gene in the absence of Gln3 in that genetic background; and (iii) the gene chosen as a reporter is able to be transcribed by Gln3 or Gat1 in the absence of the other GATA factor. Together, the data indicate that in the absence of these three pieces of information, overall NCR-sensitive gene transcription data are unreliable as Tor pathway readouts.</div>
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<Abstract><AbstractText>Nitrogen catabolite repression (NCR)-sensitive genes, whose expression is highly repressed when provided with excess nitrogen and derepressed when nitrogen is limited or cells are treated with rapamycin, are routinely used as reporters in mechanistic studies of the Tor signal transduction pathway in Saccharomyces cerevisiae. Two GATA factors, Gln3 and Gat1, are responsible for NCR-sensitive transcription, but recent evidence demonstrates that Tor pathway regulation of NCR-sensitive transcription bifurcates at the level of GATA factor localization. Gln3 requires Sit4 phosphatase for nuclear localization and NCR-sensitive transcription while Gat1 does not. In this article, we demonstrate that the extent to which Sit4 plays a role in NCR-sensitive transcription depends upon whether or not (i) Gzf3, a GATA repressor homologous to Dal80, is active in the genetic background assayed; (ii) Gat1 is able to activate transcription of the assayed gene in the absence of Gln3 in that genetic background; and (iii) the gene chosen as a reporter is able to be transcribed by Gln3 or Gat1 in the absence of the other GATA factor. Together, the data indicate that in the absence of these three pieces of information, overall NCR-sensitive gene transcription data are unreliable as Tor pathway readouts.</AbstractText>
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Nitrogen catabolite repression-sensitive transcription as a readout of Tor pathway regulation: the genetic background, reporter gene and GATA factor assayed determine the outcomes.

Nitrogen catabolite repression-sensitive transcription as a readout of Tor pathway regulation: the genetic background, reporter gene and GATA factor assayed determine the outcomes.

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