Identification of direct and indirect targets of the Gln3 and Gat1 activators by transcriptional profiling in response to nitrogen availability in the short and long term.
Identifieur interne : 001780 ( Main/Exploration ); précédent : 001779; suivant : 001781Identification of direct and indirect targets of the Gln3 and Gat1 activators by transcriptional profiling in response to nitrogen availability in the short and long term.
Auteurs : Bart Scherens [Belgique] ; André Feller ; Fabienne Vierendeels ; Francine Messenguy ; Evelyne DuboisSource :
- FEMS yeast research [ 1567-1356 ] ; 2006.
Descripteurs français
- KwdFr :
- Analyse de profil d'expression de gènes (MeSH), Azote (métabolisme), Facteurs de transcription (physiologie), Facteurs de transcription GATA (métabolisme), Facteurs de transcription GATA (physiologie), Glutamine (métabolisme), Glutathione peroxidase (MeSH), Prions (physiologie), Proline (métabolisme), Protéines de Saccharomyces cerevisiae (physiologie), Protéines de répression (physiologie), Protéines ribosomiques (génétique), Régions promotrices (génétique) (MeSH), Régulation de l'expression des gènes fongiques (MeSH), Saccharomyces cerevisiae (génétique), Saccharomyces cerevisiae (métabolisme), Sirolimus (pharmacologie), Sites de fixation (MeSH), Séquençage par oligonucléotides en batterie (MeSH).
- MESH :
- génétique : Protéines ribosomiques, Saccharomyces cerevisiae.
- métabolisme : Azote, Facteurs de transcription GATA, Glutamine, Proline, Saccharomyces cerevisiae.
- pharmacologie : Sirolimus.
- physiologie : Facteurs de transcription, Facteurs de transcription GATA, Prions, Protéines de Saccharomyces cerevisiae, Protéines de répression.
- Analyse de profil d'expression de gènes, Glutathione peroxidase, Régions promotrices (génétique), Régulation de l'expression des gènes fongiques, Sites de fixation, Séquençage par oligonucléotides en batterie.
English descriptors
- KwdEn :
- Binding Sites (MeSH), GATA Transcription Factors (metabolism), GATA Transcription Factors (physiology), Gene Expression Profiling (MeSH), Gene Expression Regulation, Fungal (MeSH), Glutamine (metabolism), Glutathione Peroxidase (MeSH), Nitrogen (metabolism), Oligonucleotide Array Sequence Analysis (MeSH), Prions (physiology), Proline (metabolism), Promoter Regions, Genetic (MeSH), Repressor Proteins (physiology), Ribosomal Proteins (genetics), Saccharomyces cerevisiae (genetics), Saccharomyces cerevisiae (metabolism), Saccharomyces cerevisiae Proteins (physiology), Sirolimus (pharmacology), Transcription Factors (physiology).
- MESH :
- chemical , genetics : Ribosomal Proteins.
- chemical , metabolism : GATA Transcription Factors, Glutamine, Nitrogen, Proline.
- chemical , pharmacology : Sirolimus.
- chemical , physiology : GATA Transcription Factors, Prions, Repressor Proteins, Saccharomyces cerevisiae Proteins, Transcription Factors.
- genetics : Saccharomyces cerevisiae.
- metabolism : Saccharomyces cerevisiae.
- Binding Sites, Gene Expression Profiling, Gene Expression Regulation, Fungal, Glutathione Peroxidase, Oligonucleotide Array Sequence Analysis, Promoter Regions, Genetic.
Abstract
Nitrogen catabolite repression (NCR) consists in the specific inhibition of transcriptional activation of genes encoding the permeases and catabolic enzymes needed to degrade poor nitrogen sources. Under nitrogen limitation or rapamycin treatment, NCR genes are activated by Gln3 or Gat1, or by both factors. To compare the sets of genes responding to rapamycin or to nitrogen limitation, we used DNA microarrays to establishing the expression profiles of a wild type strain, and of a double gln3Delta-gat1Delta strain, grown on glutamine, after addition of rapamycin, on proline, or after a shift from glutamine to proline. Analysis of microarray data revealed 392 genes whose expression was dependent on the nitrogen source quality. 91 genes were activated in a GATA factor-dependent manner in all growth conditions, suggesting a direct role of Gln3 and Gat1 in their expression. Other genes were only transiently up-regulated (stress-responsive genes) or down-regulated (genes encoding ribosomal proteins and translational factors) upon nitrogen limitation, and this regulation was delayed in a gln3Delta-gat1Delta strain. Repression of amino acid and nucleotide biosynthetic genes after a nitrogen shift did not depend on Gcn4. Several transporter genes were repressed as a consequence of enhanced levels of NCR-responsive permeases present at the plasma membrane.
DOI: 10.1111/j.1567-1364.2006.00060.x
PubMed: 16879428
Affiliations:
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xml:lang="en"><term>Saccharomyces cerevisiae</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Azote</term><term>Facteurs de transcription GATA</term><term>Glutamine</term><term>Proline</term><term>Saccharomyces cerevisiae</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Sirolimus</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Facteurs de transcription</term><term>Facteurs de transcription GATA</term><term>Prions</term><term>Protéines de Saccharomyces cerevisiae</term><term>Protéines de répression</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Binding Sites</term><term>Gene Expression Profiling</term><term>Gene Expression Regulation, Fungal</term><term>Glutathione Peroxidase</term><term>Oligonucleotide Array Sequence Analysis</term><term>Promoter Regions, Genetic</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Analyse de profil d'expression de gènes</term><term>Glutathione peroxidase</term><term>Régions promotrices (génétique)</term><term>Régulation de l'expression des gènes fongiques</term><term>Sites de fixation</term><term>Séquençage par oligonucléotides en batterie</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Nitrogen catabolite repression (NCR) consists in the specific inhibition of transcriptional activation of genes encoding the permeases and catabolic enzymes needed to degrade poor nitrogen sources. Under nitrogen limitation or rapamycin treatment, NCR genes are activated by Gln3 or Gat1, or by both factors. To compare the sets of genes responding to rapamycin or to nitrogen limitation, we used DNA microarrays to establishing the expression profiles of a wild type strain, and of a double gln3Delta-gat1Delta strain, grown on glutamine, after addition of rapamycin, on proline, or after a shift from glutamine to proline. Analysis of microarray data revealed 392 genes whose expression was dependent on the nitrogen source quality. 91 genes were activated in a GATA factor-dependent manner in all growth conditions, suggesting a direct role of Gln3 and Gat1 in their expression. Other genes were only transiently up-regulated (stress-responsive genes) or down-regulated (genes encoding ribosomal proteins and translational factors) upon nitrogen limitation, and this regulation was delayed in a gln3Delta-gat1Delta strain. Repression of amino acid and nucleotide biosynthetic genes after a nitrogen shift did not depend on Gcn4. Several transporter genes were repressed as a consequence of enhanced levels of NCR-responsive permeases present at the plasma membrane.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">16879428</PMID><DateCompleted><Year>2006</Year><Month>09</Month><Day>14</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">1567-1356</ISSN><JournalIssue CitedMedium="Print"><Volume>6</Volume><Issue>5</Issue><PubDate><Year>2006</Year><Month>Aug</Month></PubDate></JournalIssue><Title>FEMS yeast research</Title><ISOAbbreviation>FEMS Yeast Res</ISOAbbreviation></Journal><ArticleTitle>Identification of direct and indirect targets of the Gln3 and Gat1 activators by transcriptional profiling in response to nitrogen availability in the short and long term.</ArticleTitle><Pagination><MedlinePgn>777-91</MedlinePgn></Pagination><Abstract><AbstractText>Nitrogen catabolite repression (NCR) consists in the specific inhibition of transcriptional activation of genes encoding the permeases and catabolic enzymes needed to degrade poor nitrogen sources. Under nitrogen limitation or rapamycin treatment, NCR genes are activated by Gln3 or Gat1, or by both factors. To compare the sets of genes responding to rapamycin or to nitrogen limitation, we used DNA microarrays to establishing the expression profiles of a wild type strain, and of a double gln3Delta-gat1Delta strain, grown on glutamine, after addition of rapamycin, on proline, or after a shift from glutamine to proline. Analysis of microarray data revealed 392 genes whose expression was dependent on the nitrogen source quality. 91 genes were activated in a GATA factor-dependent manner in all growth conditions, suggesting a direct role of Gln3 and Gat1 in their expression. Other genes were only transiently up-regulated (stress-responsive genes) or down-regulated (genes encoding ribosomal proteins and translational factors) upon nitrogen limitation, and this regulation was delayed in a gln3Delta-gat1Delta strain. Repression of amino acid and nucleotide biosynthetic genes after a nitrogen shift did not depend on Gcn4. Several transporter genes were repressed as a consequence of enhanced levels of NCR-responsive permeases present at the plasma membrane.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Scherens</LastName><ForeName>Bart</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Institut de Recherches Microbiologiques J-M Wiame, and Laboratoire de Microbiologie, Université Libre de Bruxelles, Brussels, Belgium.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Feller</LastName><ForeName>André</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Vierendeels</LastName><ForeName>Fabienne</ForeName><Initials>F</Initials></Author><Author ValidYN="Y"><LastName>Messenguy</LastName><ForeName>Francine</ForeName><Initials>F</Initials></Author><Author ValidYN="Y"><LastName>Dubois</LastName><ForeName>Evelyne</ForeName><Initials>E</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType 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Genetic</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012097" MajorTopicYN="N">Repressor Proteins</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012269" MajorTopicYN="N">Ribosomal Proteins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012441" MajorTopicYN="N">Saccharomyces cerevisiae</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D029701" MajorTopicYN="N">Saccharomyces cerevisiae Proteins</DescriptorName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020123" MajorTopicYN="N">Sirolimus</DescriptorName><QualifierName UI="Q000494" 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IdType="doi">10.1111/j.1567-1364.2006.00060.x</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Belgique</li></country><region><li>Région de Bruxelles-Capitale</li></region><settlement><li>Bruxelles</li></settlement><orgName><li>Université libre de Bruxelles</li></orgName></list><tree><noCountry><name sortKey="Dubois, Evelyne" sort="Dubois, Evelyne" uniqKey="Dubois E" first="Evelyne" last="Dubois">Evelyne Dubois</name><name sortKey="Feller, Andre" sort="Feller, Andre" uniqKey="Feller A" first="André" last="Feller">André Feller</name><name sortKey="Messenguy, Francine" sort="Messenguy, Francine" uniqKey="Messenguy F" first="Francine" last="Messenguy">Francine Messenguy</name><name sortKey="Vierendeels, Fabienne" sort="Vierendeels, Fabienne" uniqKey="Vierendeels F" first="Fabienne" last="Vierendeels">Fabienne Vierendeels</name></noCountry><country name="Belgique"><region name="Région de Bruxelles-Capitale"><name sortKey="Scherens, Bart" sort="Scherens, Bart" uniqKey="Scherens B" first="Bart" last="Scherens">Bart Scherens</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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