Accounting for strain-specific differences during RTG target gene regulation in Saccharomyces cerevisiae.
Identifieur interne : 001801 ( Main/Exploration ); précédent : 001800; suivant : 001802Accounting for strain-specific differences during RTG target gene regulation in Saccharomyces cerevisiae.
Auteurs : Ivanka Dilova [États-Unis] ; Ted PowersSource :
- FEMS yeast research [ 1567-1356 ] ; 2006.
Descripteurs français
- KwdFr :
- Antifongiques (pharmacologie), Facteurs de transcription (génétique), Facteurs de transcription (métabolisme), Facteurs de transcription à motifs basiques hélice-boucle-hélice et à glissière à leucines (génétique), Facteurs de transcription à motifs basiques hélice-boucle-hélice et à glissière à leucines (métabolisme), Milieux de culture (MeSH), Mutation (MeSH), Phosphorylation (MeSH), Protein-Serine-Threonine Kinases (MeSH), Protéines de Saccharomyces cerevisiae (génétique), Protéines de Saccharomyces cerevisiae (métabolisme), Protéines de répression (génétique), Protéines de répression (métabolisme), Régulation de l'expression des gènes fongiques (MeSH), Saccharomyces cerevisiae (classification), Saccharomyces cerevisiae (effets des médicaments et des substances chimiques), Saccharomyces cerevisiae (génétique), Saccharomyces cerevisiae (métabolisme), Sirolimus (pharmacologie), Spécificité d'espèce (MeSH), Transduction du signal (MeSH).
- MESH :
- effets des médicaments et des substances chimiques : Saccharomyces cerevisiae.
- génétique : Facteurs de transcription, Facteurs de transcription à motifs basiques hélice-boucle-hélice et à glissière à leucines, Protéines de Saccharomyces cerevisiae, Protéines de répression, Saccharomyces cerevisiae.
- métabolisme : Facteurs de transcription, Facteurs de transcription à motifs basiques hélice-boucle-hélice et à glissière à leucines, Protéines de Saccharomyces cerevisiae, Protéines de répression, Saccharomyces cerevisiae.
- pharmacologie : Antifongiques, Sirolimus.
- Milieux de culture, Mutation, Phosphorylation, Protein-Serine-Threonine Kinases, Régulation de l'expression des gènes fongiques, Spécificité d'espèce, Transduction du signal.
English descriptors
- KwdEn :
- Antifungal Agents (pharmacology), Basic Helix-Loop-Helix Leucine Zipper Transcription Factors (genetics), Basic Helix-Loop-Helix Leucine Zipper Transcription Factors (metabolism), Culture Media (MeSH), Gene Expression Regulation, Fungal (MeSH), Mutation (MeSH), Phosphorylation (MeSH), Protein-Serine-Threonine Kinases (MeSH), Repressor Proteins (genetics), Repressor Proteins (metabolism), Saccharomyces cerevisiae (classification), Saccharomyces cerevisiae (drug effects), Saccharomyces cerevisiae (genetics), Saccharomyces cerevisiae (metabolism), Saccharomyces cerevisiae Proteins (genetics), Saccharomyces cerevisiae Proteins (metabolism), Signal Transduction (MeSH), Sirolimus (pharmacology), Species Specificity (MeSH), Transcription Factors (genetics), Transcription Factors (metabolism).
- MESH :
- chemical , genetics : Basic Helix-Loop-Helix Leucine Zipper Transcription Factors, Repressor Proteins, Saccharomyces cerevisiae Proteins, Transcription Factors.
- chemical , metabolism : Basic Helix-Loop-Helix Leucine Zipper Transcription Factors, Repressor Proteins, Saccharomyces cerevisiae Proteins, Transcription Factors.
- chemical , pharmacology : Antifungal Agents, Sirolimus.
- chemical : Culture Media, Protein-Serine-Threonine Kinases.
- classification : Saccharomyces cerevisiae.
- drug effects : Saccharomyces cerevisiae.
- genetics : Saccharomyces cerevisiae.
- metabolism : Saccharomyces cerevisiae.
- Gene Expression Regulation, Fungal, Mutation, Phosphorylation, Signal Transduction, Species Specificity.
Abstract
Mitochondrial dysfunction results in the expression, via the retrograde response pathway, of a concise set of genes (RTG target genes) that encode enzymes involved in the anapleurotic production of alpha-ketoglutarate. Inhibiting the rapamycin-sensitive TOR kinases, important regulators of cell growth, similarly results in RTG target gene expression under rich nutrient conditions. Retrograde and TOR-dependent regulation of RTG target genes requires a number of shared components, including the heterodimeric bZip/HLH transcription factors Rtg1p and Rtg3p, as well as their upstream regulator Mks1p. Two unresolved discrepancies exist with regard to the mechanism of RTG target gene control: (1) deletion of MKS1 results in constitutive expression of RTG target genes in most but not all strain backgrounds; and (2) RTG target gene expression has been correlated with both decreased as well as increased Rtg3p phosphorylation. Here we have addressed both of these issues. First, we demonstrate that the mks1 deletion strain used in a previous study by Shamji and coworkers contains a nonsense mutation within codon Ser 231 in RTG3 that likely accounts for the inactivity of the RTG system in this strain. Second, we confirm results by Butow and coworkers that Rtg3p is dephosphorylated as a primary response to induction of the pathway. Hyper-phosphorylation of this protein appears to be a secondary consequence of rapamycin treatment and is influenced both by strain background as well as by specific supplied nutrients. That hyper-phosphorylation of Rtg3p is also caused by heat shock suggests that it may reflect a more generalized response to cell stress. Together these results contribute toward a uniform view of RTG target gene regulation.
DOI: 10.1111/j.1567-1364.2005.00008.x
PubMed: 16423076
Affiliations:
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Le document en format XML
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Center for Genetics and Development, College of Biological Sciences, University of California, Davis, CA 95616, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Section of Molecular and Cellular Biology & Center for Genetics and Development, College of Biological Sciences, University of California, Davis, CA 95616</wicri:regionArea><placeName><region type="state">Californie</region></placeName></affiliation></author><author><name sortKey="Powers, Ted" sort="Powers, Ted" uniqKey="Powers T" first="Ted" last="Powers">Ted Powers</name></author></analytic><series><title level="j">FEMS yeast research</title><idno type="ISSN">1567-1356</idno><imprint><date when="2006" type="published">2006</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Antifungal Agents (pharmacology)</term><term>Basic Helix-Loop-Helix Leucine Zipper Transcription Factors (genetics)</term><term>Basic Helix-Loop-Helix Leucine Zipper Transcription Factors (metabolism)</term><term>Culture Media (MeSH)</term><term>Gene Expression Regulation, Fungal (MeSH)</term><term>Mutation (MeSH)</term><term>Phosphorylation (MeSH)</term><term>Protein-Serine-Threonine Kinases (MeSH)</term><term>Repressor Proteins (genetics)</term><term>Repressor Proteins (metabolism)</term><term>Saccharomyces cerevisiae (classification)</term><term>Saccharomyces cerevisiae (drug effects)</term><term>Saccharomyces cerevisiae (genetics)</term><term>Saccharomyces cerevisiae (metabolism)</term><term>Saccharomyces cerevisiae Proteins (genetics)</term><term>Saccharomyces cerevisiae Proteins (metabolism)</term><term>Signal Transduction (MeSH)</term><term>Sirolimus (pharmacology)</term><term>Species Specificity (MeSH)</term><term>Transcription Factors (genetics)</term><term>Transcription Factors (metabolism)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Antifongiques (pharmacologie)</term><term>Facteurs de 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qualifier="classification" xml:lang="en"><term>Saccharomyces cerevisiae</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>Facteurs de transcription</term><term>Facteurs de transcription à motifs basiques hélice-boucle-hélice et à glissière à leucines</term><term>Protéines de Saccharomyces cerevisiae</term><term>Protéines de répression</term><term>Saccharomyces cerevisiae</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Saccharomyces cerevisiae</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Facteurs de transcription</term><term>Facteurs de transcription à motifs basiques hélice-boucle-hélice et à glissière à leucines</term><term>Protéines de Saccharomyces cerevisiae</term><term>Protéines de répression</term><term>Saccharomyces cerevisiae</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Antifongiques</term><term>Sirolimus</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Gene Expression Regulation, Fungal</term><term>Mutation</term><term>Phosphorylation</term><term>Signal Transduction</term><term>Species Specificity</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Milieux de culture</term><term>Mutation</term><term>Phosphorylation</term><term>Protein-Serine-Threonine Kinases</term><term>Régulation de l'expression des gènes fongiques</term><term>Spécificité d'espèce</term><term>Transduction du signal</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Mitochondrial dysfunction results in the expression, via the retrograde response pathway, of a concise set of genes (RTG target genes) that encode enzymes involved in the anapleurotic production of alpha-ketoglutarate. Inhibiting the rapamycin-sensitive TOR kinases, important regulators of cell growth, similarly results in RTG target gene expression under rich nutrient conditions. Retrograde and TOR-dependent regulation of RTG target genes requires a number of shared components, including the heterodimeric bZip/HLH transcription factors Rtg1p and Rtg3p, as well as their upstream regulator Mks1p. Two unresolved discrepancies exist with regard to the mechanism of RTG target gene control: (1) deletion of MKS1 results in constitutive expression of RTG target genes in most but not all strain backgrounds; and (2) RTG target gene expression has been correlated with both decreased as well as increased Rtg3p phosphorylation. Here we have addressed both of these issues. First, we demonstrate that the mks1 deletion strain used in a previous study by Shamji and coworkers contains a nonsense mutation within codon Ser 231 in RTG3 that likely accounts for the inactivity of the RTG system in this strain. Second, we confirm results by Butow and coworkers that Rtg3p is dephosphorylated as a primary response to induction of the pathway. Hyper-phosphorylation of this protein appears to be a secondary consequence of rapamycin treatment and is influenced both by strain background as well as by specific supplied nutrients. That hyper-phosphorylation of Rtg3p is also caused by heat shock suggests that it may reflect a more generalized response to cell stress. Together these results contribute toward a uniform view of RTG target gene regulation.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">16423076</PMID><DateCompleted><Year>2006</Year><Month>05</Month><Day>10</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>1</Issue><PubDate><Year>2006</Year><Month>Jan</Month></PubDate></JournalIssue><Title>FEMS yeast research</Title><ISOAbbreviation>FEMS Yeast Res</ISOAbbreviation></Journal><ArticleTitle>Accounting for strain-specific differences during RTG target gene regulation in Saccharomyces cerevisiae.</ArticleTitle><Pagination><MedlinePgn>112-9</MedlinePgn></Pagination><Abstract><AbstractText>Mitochondrial dysfunction results in the expression, via the retrograde response pathway, of a concise set of genes (RTG target genes) that encode enzymes involved in the anapleurotic production of alpha-ketoglutarate. Inhibiting the rapamycin-sensitive TOR kinases, important regulators of cell growth, similarly results in RTG target gene expression under rich nutrient conditions. Retrograde and TOR-dependent regulation of RTG target genes requires a number of shared components, including the heterodimeric bZip/HLH transcription factors Rtg1p and Rtg3p, as well as their upstream regulator Mks1p. Two unresolved discrepancies exist with regard to the mechanism of RTG target gene control: (1) deletion of MKS1 results in constitutive expression of RTG target genes in most but not all strain backgrounds; and (2) RTG target gene expression has been correlated with both decreased as well as increased Rtg3p phosphorylation. Here we have addressed both of these issues. First, we demonstrate that the mks1 deletion strain used in a previous study by Shamji and coworkers contains a nonsense mutation within codon Ser 231 in RTG3 that likely accounts for the inactivity of the RTG system in this strain. Second, we confirm results by Butow and coworkers that Rtg3p is dephosphorylated as a primary response to induction of the pathway. Hyper-phosphorylation of this protein appears to be a secondary consequence of rapamycin treatment and is influenced both by strain background as well as by specific supplied nutrients. That hyper-phosphorylation of Rtg3p is also caused by heat shock suggests that it may reflect a more generalized response to cell stress. Together these results contribute toward a uniform view of RTG target gene regulation.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Dilova</LastName><ForeName>Ivanka</ForeName><Initials>I</Initials><AffiliationInfo><Affiliation>Section of Molecular and Cellular Biology & Center for Genetics and Development, College of Biological Sciences, University of California, Davis, CA 95616, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Powers</LastName><ForeName>Ted</ForeName><Initials>T</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013486">Research Support, U.S. Gov't, Non-P.H.S.</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>FEMS Yeast 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cerevisiae</DescriptorName><QualifierName UI="Q000145" MajorTopicYN="Y">classification</QualifierName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D029701" MajorTopicYN="N">Saccharomyces cerevisiae Proteins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020123" MajorTopicYN="N">Sirolimus</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013045" MajorTopicYN="N">Species Specificity</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014157" MajorTopicYN="N">Transcription Factors</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2006</Year><Month>1</Month><Day>21</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2006</Year><Month>5</Month><Day>11</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2006</Year><Month>1</Month><Day>21</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">16423076</ArticleId><ArticleId IdType="pii">FYR008</ArticleId><ArticleId IdType="doi">10.1111/j.1567-1364.2005.00008.x</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>États-Unis</li></country><region><li>Californie</li></region></list><tree><noCountry><name sortKey="Powers, Ted" sort="Powers, Ted" uniqKey="Powers T" first="Ted" last="Powers">Ted Powers</name></noCountry><country name="États-Unis"><region name="Californie"><name sortKey="Dilova, Ivanka" sort="Dilova, Ivanka" uniqKey="Dilova I" first="Ivanka" last="Dilova">Ivanka Dilova</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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