Loss of the TOR kinase Tor2 mimics nitrogen starvation and activates the sexual development pathway in fission yeast.
Identifieur interne : 001715 ( Main/Exploration ); précédent : 001714; suivant : 001716Loss of the TOR kinase Tor2 mimics nitrogen starvation and activates the sexual development pathway in fission yeast.
Auteurs : Tomohiko Matsuo [Japon] ; Yoko Otsubo ; Jun Urano ; Fuyuhiko Tamanoi ; Masayuki YamamotoSource :
- Molecular and cellular biology [ 0270-7306 ] ; 2007.
Descripteurs français
- KwdFr :
- Analyse de profil d'expression de gènes (MeSH), Azote (métabolisme), Développement sexuel (physiologie), Gènes fongiques du type conjugant (MeSH), Liaison aux protéines (MeSH), Méiose (MeSH), Phase G1 (MeSH), Phosphatidylinositol 3-kinases (déficit), Phosphatidylinositol 3-kinases (métabolisme), Phénotype (MeSH), Protéines de Schizosaccharomyces pombe (génétique), Protéines de Schizosaccharomyces pombe (métabolisme), Protéines de transport membranaire (génétique), Protéines mutantes (isolement et purification), Régulation de l'expression des gènes fongiques (MeSH), Schizosaccharomyces (cytologie), Schizosaccharomyces (enzymologie), Schizosaccharomyces (génétique), Séquençage par oligonucléotides en batterie (MeSH).
- MESH :
- cytologie : Schizosaccharomyces.
- déficit : Phosphatidylinositol 3-kinases.
- enzymologie : Schizosaccharomyces.
- génétique : Protéines de Schizosaccharomyces pombe, Protéines de transport membranaire, Schizosaccharomyces.
- isolement et purification : Protéines mutantes.
- métabolisme : Azote, Phosphatidylinositol 3-kinases, Protéines de Schizosaccharomyces pombe.
- physiologie : Développement sexuel.
- Analyse de profil d'expression de gènes, Gènes fongiques du type conjugant, Liaison aux protéines, Méiose, Phase G1, Phénotype, Régulation de l'expression des gènes fongiques, Séquençage par oligonucléotides en batterie.
English descriptors
- KwdEn :
- G1 Phase (MeSH), Gene Expression Profiling (MeSH), Gene Expression Regulation, Fungal (MeSH), Genes, Mating Type, Fungal (MeSH), Meiosis (MeSH), Membrane Transport Proteins (genetics), Mutant Proteins (isolation & purification), Nitrogen (metabolism), Oligonucleotide Array Sequence Analysis (MeSH), Phenotype (MeSH), Phosphatidylinositol 3-Kinases (deficiency), Phosphatidylinositol 3-Kinases (metabolism), Protein Binding (MeSH), Schizosaccharomyces (cytology), Schizosaccharomyces (enzymology), Schizosaccharomyces (genetics), Schizosaccharomyces pombe Proteins (genetics), Schizosaccharomyces pombe Proteins (metabolism), Sexual Development (physiology).
- MESH :
- chemical , deficiency : Phosphatidylinositol 3-Kinases.
- chemical , genetics : Membrane Transport Proteins, Schizosaccharomyces pombe Proteins.
- chemical , isolation & purification : Mutant Proteins.
- chemical , metabolism : Nitrogen, Phosphatidylinositol 3-Kinases, Schizosaccharomyces pombe Proteins.
- cytology : Schizosaccharomyces.
- enzymology : Schizosaccharomyces.
- genetics : Schizosaccharomyces.
- physiology : Sexual Development.
- G1 Phase, Gene Expression Profiling, Gene Expression Regulation, Fungal, Genes, Mating Type, Fungal, Meiosis, Oligonucleotide Array Sequence Analysis, Phenotype, Protein Binding.
Abstract
Fission yeast has two TOR (target of rapamycin) kinases, namely Tor1 and Tor2. Tor1 is required for survival under stressed conditions, proper G(1) arrest, and sexual development. In contrast, Tor2 is essential for growth. To analyze the functions of Tor2, we constructed two temperature-sensitive tor2 mutants. Interestingly, at the restrictive temperature, these mutants mimicked nitrogen starvation by arresting the cell cycle in G(1) phase and initiating sexual development. Microarray analysis indicated that expression of nitrogen starvation-responsive genes was induced extensively when Tor2 function was suppressed, suggesting that Tor2 normally mediates a signal from the nitrogen source. As with mammalian and budding yeast TOR, we find that fission yeast TOR also forms multiprotein complexes analogous to TORC1 and TORC2. The raptor homologue, Mip1, likely forms a complex predominantly with Tor2, producing TORC1. The rictor/Avo3 homologue, Ste20, and the Avo1 homologue, Sin1, appear to form TORC2 mainly with Tor1 but may also bind Tor2. The Lst8 homologue, Wat1, binds to both Tor1 and Tor2. Our analysis shows, with respect to promotion of G(1) arrest and sexual development, that the loss of Tor1 (TORC2) and the loss of Tor2 (TORC1) exhibit opposite effects. This highlights an intriguing functional relationship among TOR kinase complexes in the fission yeast Schizosaccharomyces pombe.
DOI: 10.1128/MCB.01039-06
PubMed: 17261596
PubMed Central: PMC1899950
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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Development</term></keywords><keywords scheme="MESH" xml:lang="en"><term>G1 Phase</term><term>Gene Expression Profiling</term><term>Gene Expression Regulation, Fungal</term><term>Genes, Mating Type, Fungal</term><term>Meiosis</term><term>Oligonucleotide Array Sequence Analysis</term><term>Phenotype</term><term>Protein Binding</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Analyse de profil d'expression de gènes</term><term>Gènes fongiques du type conjugant</term><term>Liaison aux protéines</term><term>Méiose</term><term>Phase G1</term><term>Phénotype</term><term>Régulation de l'expression des gènes fongiques</term><term>Séquençage par oligonucléotides en batterie</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Fission yeast has two TOR (target of rapamycin) kinases, namely Tor1 and Tor2. Tor1 is required for survival under stressed conditions, proper G(1) arrest, and sexual development. In contrast, Tor2 is essential for growth. To analyze the functions of Tor2, we constructed two temperature-sensitive tor2 mutants. Interestingly, at the restrictive temperature, these mutants mimicked nitrogen starvation by arresting the cell cycle in G(1) phase and initiating sexual development. Microarray analysis indicated that expression of nitrogen starvation-responsive genes was induced extensively when Tor2 function was suppressed, suggesting that Tor2 normally mediates a signal from the nitrogen source. As with mammalian and budding yeast TOR, we find that fission yeast TOR also forms multiprotein complexes analogous to TORC1 and TORC2. The raptor homologue, Mip1, likely forms a complex predominantly with Tor2, producing TORC1. The rictor/Avo3 homologue, Ste20, and the Avo1 homologue, Sin1, appear to form TORC2 mainly with Tor1 but may also bind Tor2. The Lst8 homologue, Wat1, binds to both Tor1 and Tor2. Our analysis shows, with respect to promotion of G(1) arrest and sexual development, that the loss of Tor1 (TORC2) and the loss of Tor2 (TORC1) exhibit opposite effects. This highlights an intriguing functional relationship among TOR kinase complexes in the fission yeast Schizosaccharomyces pombe.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">17261596</PMID><DateCompleted><Year>2007</Year><Month>05</Month><Day>08</Day></DateCompleted><DateRevised><Year>2018</Year><Month>12</Month><Day>27</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Print">0270-7306</ISSN><JournalIssue CitedMedium="Print"><Volume>27</Volume><Issue>8</Issue><PubDate><Year>2007</Year><Month>Apr</Month></PubDate></JournalIssue><Title>Molecular and cellular biology</Title><ISOAbbreviation>Mol Cell Biol</ISOAbbreviation></Journal><ArticleTitle>Loss of the TOR kinase Tor2 mimics nitrogen starvation and activates the sexual development pathway in fission yeast.</ArticleTitle><Pagination><MedlinePgn>3154-64</MedlinePgn></Pagination><Abstract><AbstractText>Fission yeast has two TOR (target of rapamycin) kinases, namely Tor1 and Tor2. Tor1 is required for survival under stressed conditions, proper G(1) arrest, and sexual development. In contrast, Tor2 is essential for growth. To analyze the functions of Tor2, we constructed two temperature-sensitive tor2 mutants. Interestingly, at the restrictive temperature, these mutants mimicked nitrogen starvation by arresting the cell cycle in G(1) phase and initiating sexual development. Microarray analysis indicated that expression of nitrogen starvation-responsive genes was induced extensively when Tor2 function was suppressed, suggesting that Tor2 normally mediates a signal from the nitrogen source. As with mammalian and budding yeast TOR, we find that fission yeast TOR also forms multiprotein complexes analogous to TORC1 and TORC2. The raptor homologue, Mip1, likely forms a complex predominantly with Tor2, producing TORC1. The rictor/Avo3 homologue, Ste20, and the Avo1 homologue, Sin1, appear to form TORC2 mainly with Tor1 but may also bind Tor2. The Lst8 homologue, Wat1, binds to both Tor1 and Tor2. Our analysis shows, with respect to promotion of G(1) arrest and sexual development, that the loss of Tor1 (TORC2) and the loss of Tor2 (TORC1) exhibit opposite effects. This highlights an intriguing functional relationship among TOR kinase complexes in the fission yeast Schizosaccharomyces pombe.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Matsuo</LastName><ForeName>Tomohiko</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Department of Biophysics and Biochemistry, Graduate School of Science, University of Tokyo, Tokyo 113-0033, Japan. yamamoto@biochem.s.u-tokyo.ac.jp</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Otsubo</LastName><ForeName>Yoko</ForeName><Initials>Y</Initials></Author><Author ValidYN="Y"><LastName>Urano</LastName><ForeName>Jun</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Tamanoi</LastName><ForeName>Fuyuhiko</ForeName><Initials>F</Initials></Author><Author ValidYN="Y"><LastName>Yamamoto</LastName><ForeName>Masayuki</ForeName><Initials>M</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01 CA041996</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>CA41996</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D013486">Research Support, U.S. Gov't, Non-P.H.S.</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2007</Year><Month>01</Month><Day>29</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mol Cell Biol</MedlineTA><NlmUniqueID>8109087</NlmUniqueID><ISSNLinking>0270-7306</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D026901">Membrane Transport Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D050505">Mutant Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D029702">Schizosaccharomyces pombe Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.1.-</RegistryNumber><NameOfSubstance UI="D019869">Phosphatidylinositol 3-Kinases</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.1.137</RegistryNumber><NameOfSubstance UI="C513100">tor2 protein, S pombe</NameOfSubstance></Chemical><Chemical><RegistryNumber>N762921K75</RegistryNumber><NameOfSubstance UI="D009584">Nitrogen</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D016193" MajorTopicYN="N">G1 Phase</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020869" MajorTopicYN="N">Gene Expression Profiling</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015966" MajorTopicYN="N">Gene Expression Regulation, Fungal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D049770" MajorTopicYN="N">Genes, Mating Type, Fungal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008540" MajorTopicYN="N">Meiosis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D026901" MajorTopicYN="N">Membrane Transport Proteins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D050505" MajorTopicYN="N">Mutant Proteins</DescriptorName><QualifierName UI="Q000302" MajorTopicYN="N">isolation & purification</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009584" MajorTopicYN="N">Nitrogen</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020411" MajorTopicYN="N">Oligonucleotide Array Sequence Analysis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010641" MajorTopicYN="N">Phenotype</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D019869" MajorTopicYN="N">Phosphatidylinositol 3-Kinases</DescriptorName><QualifierName UI="Q000172" MajorTopicYN="Y">deficiency</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011485" MajorTopicYN="N">Protein Binding</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012568" MajorTopicYN="N">Schizosaccharomyces</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName><QualifierName UI="Q000201" MajorTopicYN="Y">enzymology</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D029702" MajorTopicYN="N">Schizosaccharomyces pombe Proteins</DescriptorName><QualifierName UI="Q000235" 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Masayuki" sort="Yamamoto, Masayuki" uniqKey="Yamamoto M" first="Masayuki" last="Yamamoto">Masayuki Yamamoto</name></noCountry><country name="Japon"><region name="Région de Kantō"><name sortKey="Matsuo, Tomohiko" sort="Matsuo, Tomohiko" uniqKey="Matsuo T" first="Tomohiko" last="Matsuo">Tomohiko Matsuo</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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