Thioredoxin deficiency in yeast prolongs S phase and shortens the G1 interval of the cell cycle.
Identifieur interne : 001292 ( Main/Exploration ); précédent : 001291; suivant : 001293Thioredoxin deficiency in yeast prolongs S phase and shortens the G1 interval of the cell cycle.
Auteurs : E G Muller [États-Unis]Source :
- The Journal of biological chemistry [ 0021-9258 ] ; 1991.
Descripteurs français
- KwdFr :
- Cartographie de restriction (MeSH), Clonage moléculaire (MeSH), Cycle cellulaire (MeSH), Données de séquences moléculaires (MeSH), Délétion de segment de chromosome (MeSH), Gènes fongiques (MeSH), Oligonucléotides (composition chimique), Phase S (MeSH), Saccharomyces cerevisiae (cytologie), Saccharomyces cerevisiae (génétique), Séquence nucléotidique (MeSH), Thiorédoxines (génétique), Thiorédoxines (métabolisme).
- MESH :
- composition chimique : Oligonucléotides.
- cytologie : Saccharomyces cerevisiae.
- génétique : Saccharomyces cerevisiae, Thiorédoxines.
- métabolisme : Thiorédoxines.
- Cartographie de restriction, Clonage moléculaire, Cycle cellulaire, Données de séquences moléculaires, Délétion de segment de chromosome, Gènes fongiques, Phase S, Séquence nucléotidique.
English descriptors
- KwdEn :
- Base Sequence (MeSH), Cell Cycle (MeSH), Chromosome Deletion (MeSH), Cloning, Molecular (MeSH), Genes, Fungal (MeSH), Molecular Sequence Data (MeSH), Oligonucleotides (chemistry), Restriction Mapping (MeSH), S Phase (MeSH), Saccharomyces cerevisiae (cytology), Saccharomyces cerevisiae (genetics), Thioredoxins (genetics), Thioredoxins (metabolism).
- MESH :
- chemical , chemistry : Oligonucleotides.
- cytology : Saccharomyces cerevisiae.
- genetics : Saccharomyces cerevisiae, Thioredoxins.
- chemical , metabolism : Thioredoxins.
- Base Sequence, Cell Cycle, Chromosome Deletion, Cloning, Molecular, Genes, Fungal, Molecular Sequence Data, Restriction Mapping, S Phase.
Abstract
Two thioredoxin genes from the yeast Saccharomyces cerevisiae were cloned using synthetic oligonucleotide probes. The DNA sequences of the two genes were found to be 74% identical. The two genes, designated TRX1 and TRX2, were mutagenized in vitro and used to construct a set of thioredoxin deletion mutants. The loss of either thioredoxin gene alone has no effect on cell growth or morphology. However, the simultaneous deletion of both thioredoxin genes profoundly affects the cell cycle. S phase is 3-fold longer, and G1 is virtually absent. In addition, the thioredoxin double mutant shows a 33% increase in generation time, a significant increase in cell size, and a greater proportion of large budded cells. The results suggest that in the absence of TRX1 and TRX2, a slow rate of DNA replication inhibits the normal progress of cellular reproduction. Surprisingly, the loss of both thioredoxins also leads to methionine auxotrophy. Thus yeast glutaredoxin is unable to substitute for thioredoxin in sulfate assimilation. As a first step in studying the cell cycle control mechanisms that respond to the thioredoxin deficiency, it was shown that cell viability does not require the function of RAD9, a known cell cycle checkpoint.
PubMed: 2026619
Affiliations:
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Le document en format XML
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The DNA sequences of the two genes were found to be 74% identical. The two genes, designated TRX1 and TRX2, were mutagenized in vitro and used to construct a set of thioredoxin deletion mutants. The loss of either thioredoxin gene alone has no effect on cell growth or morphology. However, the simultaneous deletion of both thioredoxin genes profoundly affects the cell cycle. S phase is 3-fold longer, and G1 is virtually absent. In addition, the thioredoxin double mutant shows a 33% increase in generation time, a significant increase in cell size, and a greater proportion of large budded cells. The results suggest that in the absence of TRX1 and TRX2, a slow rate of DNA replication inhibits the normal progress of cellular reproduction. Surprisingly, the loss of both thioredoxins also leads to methionine auxotrophy. Thus yeast glutaredoxin is unable to substitute for thioredoxin in sulfate assimilation. As a first step in studying the cell cycle control mechanisms that respond to the thioredoxin deficiency, it was shown that cell viability does not require the function of RAD9, a known cell cycle checkpoint.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">2026619</PMID><DateCompleted><Year>1991</Year><Month>06</Month><Day>10</Day></DateCompleted><DateRevised><Year>2007</Year><Month>11</Month><Day>15</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0021-9258</ISSN><JournalIssue CitedMedium="Print"><Volume>266</Volume><Issue>14</Issue><PubDate><Year>1991</Year><Month>May</Month><Day>15</Day></PubDate></JournalIssue><Title>The Journal of biological chemistry</Title><ISOAbbreviation>J Biol Chem</ISOAbbreviation></Journal><ArticleTitle>Thioredoxin deficiency in yeast prolongs S phase and shortens the G1 interval of the cell cycle.</ArticleTitle><Pagination><MedlinePgn>9194-202</MedlinePgn></Pagination><Abstract><AbstractText>Two thioredoxin genes from the yeast Saccharomyces cerevisiae were cloned using synthetic oligonucleotide probes. The DNA sequences of the two genes were found to be 74% identical. The two genes, designated TRX1 and TRX2, were mutagenized in vitro and used to construct a set of thioredoxin deletion mutants. The loss of either thioredoxin gene alone has no effect on cell growth or morphology. However, the simultaneous deletion of both thioredoxin genes profoundly affects the cell cycle. S phase is 3-fold longer, and G1 is virtually absent. In addition, the thioredoxin double mutant shows a 33% increase in generation time, a significant increase in cell size, and a greater proportion of large budded cells. The results suggest that in the absence of TRX1 and TRX2, a slow rate of DNA replication inhibits the normal progress of cellular reproduction. Surprisingly, the loss of both thioredoxins also leads to methionine auxotrophy. Thus yeast glutaredoxin is unable to substitute for thioredoxin in sulfate assimilation. As a first step in studying the cell cycle control mechanisms that respond to the thioredoxin deficiency, it was shown that cell viability does not require the function of RAD9, a known cell cycle checkpoint.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Muller</LastName><ForeName>E G</ForeName><Initials>EG</Initials><AffiliationInfo><Affiliation>Department of Biochemistry, University of Washington, Seattle, 98195.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><DataBankList CompleteYN="Y"><DataBank><DataBankName>GENBANK</DataBankName><AccessionNumberList><AccessionNumber>M57623</AccessionNumber><AccessionNumber>M57624</AccessionNumber><AccessionNumber>M60203</AccessionNumber><AccessionNumber>M60204</AccessionNumber><AccessionNumber>M60205</AccessionNumber><AccessionNumber>M60206</AccessionNumber><AccessionNumber>M62647</AccessionNumber><AccessionNumber>M62648</AccessionNumber><AccessionNumber>M62780</AccessionNumber><AccessionNumber>M63262</AccessionNumber></AccessionNumberList></DataBank></DataBankList><GrantList CompleteYN="Y"><Grant><GrantID>GM45448</GrantID><Acronym>GM</Acronym><Agency>NIGMS NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D003160">Comparative Study</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D013487">Research Support, U.S. Gov't, P.H.S.</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Biol Chem</MedlineTA><NlmUniqueID>2985121R</NlmUniqueID><ISSNLinking>0021-9258</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D009841">Oligonucleotides</NameOfSubstance></Chemical><Chemical><RegistryNumber>52500-60-4</RegistryNumber><NameOfSubstance UI="D013879">Thioredoxins</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><GeneSymbolList><GeneSymbol>RAD6</GeneSymbol><GeneSymbol>TRX1</GeneSymbol><GeneSymbol>TRX2</GeneSymbol></GeneSymbolList><MeshHeadingList><MeshHeading><DescriptorName UI="D001483" MajorTopicYN="N">Base Sequence</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002453" MajorTopicYN="Y">Cell Cycle</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002872" MajorTopicYN="N">Chromosome Deletion</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003001" MajorTopicYN="N">Cloning, Molecular</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005800" MajorTopicYN="Y">Genes, Fungal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008969" MajorTopicYN="N">Molecular Sequence Data</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009841" MajorTopicYN="N">Oligonucleotides</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015183" MajorTopicYN="N">Restriction Mapping</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016196" MajorTopicYN="N">S Phase</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012441" MajorTopicYN="N">Saccharomyces cerevisiae</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="N">cytology</QualifierName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013879" MajorTopicYN="N">Thioredoxins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1991</Year><Month>5</Month><Day>15</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1991</Year><Month>5</Month><Day>15</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1991</Year><Month>5</Month><Day>15</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">2026619</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>États-Unis</li></country><region><li>Washington (État)</li></region><settlement><li>Seattle</li></settlement><orgName><li>Université de Washington</li></orgName></list><tree><country name="États-Unis"><region name="Washington (État)"><name sortKey="Muller, E G" sort="Muller, E G" uniqKey="Muller E" first="E G" last="Muller">E G Muller</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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