The yeast UASG is a transcriptional enhancer in human hela cells in the presence of the GAL4 trans -activator
Identifieur interne : 001815 ( Istex/Corpus ); précédent : 001814; suivant : 001816The yeast UASG is a transcriptional enhancer in human hela cells in the presence of the GAL4 trans -activator
Auteurs : Nicholas Webster ; Jia Rui Jin ; Stephen Green ; Melvyn Hollis ; Pierre ChambonSource :
- Cell [ 0092-8674 ] ; 1988.
English descriptors
- Teeft :
- 1fmer, Acidic, Acidic regions, Activator, Amino, Amino acid core, Amino acids, Binding domain, Chambon, Cotransfected, Densitometric scanning, Early promoter, Efficient transcription, Enhancer, Enhancer element, Enhancer elements, Estrogen, Estrogen receptor, Eukaryote, Eukaryotic, Experimental procedures, Gal4, Gal4 binding sites, Gal4 coding sequence, Gal4 expression vector, Gcn4, Gene, Giniger, Hela, Hela cells, Higher eukaryotes, Higher eukaryotic enhancers, Human estrogen receptor, Human hela cells, Kumar, Mammalian cells, Nuclease, Nuclease analysis, Plasmid, Polylinker, Promoter, Promoter elements, Ptashne, Receptor, Reference gene, Reference gene pg1b, Reference plasmid, Reporter gene, Reporter genes, Reporter plasmids, Schematic organization, Seal site, Struhl, Tata, Transcription, Transcriptional, Transcriptional activation, Uase, Uaso, Unpublished data, Wasylyk, Yeast, Zenke.
Abstract
Abstract: The yeast trans-activator protein GAL4, when expressed in HeLa cells, stimulates transcription from several class B (II) eukaryotic promoters containing GAL4 binding sites either as the full UASG or as synthetic 17-mers. The characteristics of this activation are indistinguishable from those of the SV40 enhancer. Transcription was similarly stimulated from either complex promoter regions containing multiple upstream elements or from a simple promoter region composed of only a TATA box. Addition of a 17-mer GAL4 binding site to the SV40 enhancer resulted in a synergistic enhancement of transcription in the presence of GAL4. Furthermore, chimeras of the human estrogen receptor DNA binding domain and either GAL4 or GCN4 activating “acidic” regions can activate a promoter region controlled by an estrogen-responsive enhancer. Together, these data indicate that the molecular mechanisms responsible for transcriptional enhancement have been conserved from yeast to man.
Url:
DOI: 10.1016/0092-8674(88)90505-3
Links to Exploration step
ISTEX:F93AD5F4E6BECF17113A3C523918F4C3B276E675Le document en format XML
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regions</term><term>Activator</term><term>Amino</term><term>Amino acid core</term><term>Amino acids</term><term>Binding domain</term><term>Chambon</term><term>Cotransfected</term><term>Densitometric scanning</term><term>Early promoter</term><term>Efficient transcription</term><term>Enhancer</term><term>Enhancer element</term><term>Enhancer elements</term><term>Estrogen</term><term>Estrogen receptor</term><term>Eukaryote</term><term>Eukaryotic</term><term>Experimental procedures</term><term>Gal4</term><term>Gal4 binding sites</term><term>Gal4 coding sequence</term><term>Gal4 expression vector</term><term>Gcn4</term><term>Gene</term><term>Giniger</term><term>Hela</term><term>Hela cells</term><term>Higher eukaryotes</term><term>Higher eukaryotic enhancers</term><term>Human estrogen receptor</term><term>Human hela cells</term><term>Kumar</term><term>Mammalian cells</term><term>Nuclease</term><term>Nuclease analysis</term><term>Plasmid</term><term>Polylinker</term><term>Promoter</term><term>Promoter elements</term><term>Ptashne</term><term>Receptor</term><term>Reference gene</term><term>Reference gene pg1b</term><term>Reference plasmid</term><term>Reporter gene</term><term>Reporter genes</term><term>Reporter plasmids</term><term>Schematic organization</term><term>Seal site</term><term>Struhl</term><term>Tata</term><term>Transcription</term><term>Transcriptional</term><term>Transcriptional activation</term><term>Uase</term><term>Uaso</term><term>Unpublished data</term><term>Wasylyk</term><term>Yeast</term><term>Zenke</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: The yeast trans-activator protein GAL4, when expressed in HeLa cells, stimulates transcription from several class B (II) eukaryotic promoters containing GAL4 binding sites either as the full UASG or as synthetic 17-mers. The characteristics of this activation are indistinguishable from those of the SV40 enhancer. Transcription was similarly stimulated from either complex promoter regions containing multiple upstream elements or from a simple promoter region composed of only a TATA box. Addition of a 17-mer GAL4 binding site to the SV40 enhancer resulted in a synergistic enhancement of transcription in the presence of GAL4. Furthermore, chimeras of the human estrogen receptor DNA binding domain and either GAL4 or GCN4 activating “acidic” regions can activate a promoter region controlled by an estrogen-responsive enhancer. 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The characteristics of this activation are indistinguishable from those of the SV40 enhancer. Transcription was similarly stimulated from either complex promoter regions containing multiple upstream elements or from a simple promoter region composed of only a TATA box. Addition of a 17-mer GAL4 binding site to the SV40 enhancer resulted in a synergistic enhancement of transcription in the presence of GAL4. Furthermore, chimeras of the human estrogen receptor DNA binding domain and either GAL4 or GCN4 activating “acidic” regions can activate a promoter region controlled by an estrogen-responsive enhancer. Together, these data indicate that the molecular mechanisms responsible for transcriptional enhancement have been conserved from yeast to man.</abstract><qualityIndicators><score>8.692</score><pdfWordCount>7409</pdfWordCount><pdfCharCount>47777</pdfCharCount><pdfVersion>1.3</pdfVersion><pdfPageCount>10</pdfPageCount><pdfPageSize>619 x 799 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractWordCount>141</abstractWordCount><abstractCharCount>985</abstractCharCount><keywordCount>0</keywordCount></qualityIndicators><title>The yeast UASG is a transcriptional enhancer in human hela cells in the presence of the GAL4 trans -activator</title><pmid><json:string>2830022</json:string></pmid><pii><json:string>0092-8674(88)90505-3</json:string></pii><genre><json:string>research-article</json:string></genre><serie><title>Proc. Natl. Aced. Sci. USA</title><language><json:string>unknown</json:string></language><volume>84</volume><pages><first>6795</first><last>6799</last></pages></serie><host><title>Cell</title><language><json:string>unknown</json:string></language><publicationDate>1988</publicationDate><issn><json:string>0092-8674</json:string></issn><pii><json:string>S0092-8674(00)X0420-5</json:string></pii><volume>52</volume><issue>2</issue><pages><first>169</first><last>178</last></pages><genre><json:string>journal</json:string></genre></host><namedEntities><unitex><date><json:string>1142</json:string><json:string>1988</json:string></date><geogName></geogName><orgName><json:string>Hormone Research, Volume</json:string><json:string>A Laboratory Manual</json:string><json:string>Biochem</json:string><json:string>Harvard University</json:string><json:string>National Institutes of Health</json:string><json:string>INSERM</json:string></orgName><orgName_funder><json:string>INSERM</json:string></orgName_funder><orgName_provider></orgName_provider><persName><json:string>Genes</json:string><json:string>C. Wed</json:string><json:string>M. Hollis</json:string><json:string>J. Biol</json:string><json:string>Melvyn Hollis</json:string><json:string>J. White</json:string><json:string>Stephen Green</json:string><json:string>Rui Jin</json:string><json:string>E. Scheer</json:string><json:string>Pierre Chambon</json:string><json:string>V. Kumar</json:string><json:string>B. D. Hames</json:string><json:string>U.S.C. Section</json:string><json:string>G. Ryffel</json:string><json:string>A. Staub</json:string><json:string>R. Yocum</json:string><json:string>Spring Harbor</json:string><json:string>L. Keegan</json:string><json:string>B. Boulay</json:string><json:string>F. Ruffenach</json:string><json:string>M. Ptashne</json:string></persName><placeName><json:string>Cisek</json:string><json:string>HEl</json:string><json:string>Baltimore</json:string><json:string>York</json:string><json:string>Cambridge</json:string></placeName><ref_url></ref_url><ref_bibl><json:string>Zenke et al., 1986</json:string><json:string>Schirm et al., 1987</json:string><json:string>Wasylyk et al., 1984</json:string><json:string>Bonnerot et al., 1987</json:string><json:string>Kakidani and Ptashne (1986)</json:string><json:string>Ma and Ptashne, 1987a</json:string><json:string>Ma and Ptashne (1967b)</json:string><json:string>Klein-Hitpass et al., 1966</json:string><json:string>Ptashne (1986)</json:string><json:string>Kumar et al.. 1987</json:string><json:string>see Hope and Struhl, 1986</json:string><json:string>Yocum et al., 1984</json:string><json:string>Giniger et al., 1985</json:string><json:string>Brent and Ptashne, 1985</json:string><json:string>Wasylyk et al., 1983</json:string><json:string>SassoneCorsi et al., 1985</json:string><json:string>Hen et al., 1986</json:string><json:string>Giniger and Ptashne, 1988</json:string><json:string>Barrera-Saldana et al., 1985</json:string><json:string>Takahashi et al. (1986)</json:string><json:string>Breathnach and Harris, 1983</json:string><json:string>Serfling et al., 1985</json:string><json:string>amino acids 107 to 125; see Hope and Struhl, 1966</json:string><json:string>Maniatis et al., 1962</json:string><json:string>Silver et al., 1964</json:string><json:string>Hatzopoulos et al., 1987</json:string><json:string>Kumar et al., 1987</json:string><json:string>Giniger and Ptashne, 1987</json:string><json:string>Kakidani and Ptashne (1988)</json:string><json:string>Klein-Hitpass et al., 1986</json:string><json:string>Ondek et al., 1987</json:string><json:string>Ahearn et al., 1987</json:string><json:string>Kumar et al., 1986</json:string><json:string>Nomiyama et al., 1987</json:string><json:string>Zenke et al., 1966</json:string><json:string>Keegan et al., 1986</json:string><json:string>Bram et al., 1986</json:string><json:string>Takahashi et al., 1986</json:string><json:string>Groudine et al., 1961</json:string><json:string>Maniatis et al., 1987</json:string><json:string>Ma and Ptashne, 1987b</json:string><json:string>Petkovich et al., 1987</json:string><json:string>Wirth and Baltimore, 1987</json:string><json:string>Kumar et al., 1967</json:string><json:string>Augereau and Wasylyk, 1984</json:string><json:string>Chambon et al., 1984</json:string><json:string>Hen et al., 1982</json:string></ref_bibl><bibl></bibl></unitex></namedEntities><ark><json:string>ark:/67375/6H6-BW8F0VTZ-8</json:string></ark><categories><wos><json:string>1 - 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The characteristics of this activation are indistinguishable from those of the SV40 enhancer. Transcription was similarly stimulated from either complex promoter regions containing multiple upstream elements or from a simple promoter region composed of only a TATA box. Addition of a 17-mer GAL4 binding site to the SV40 enhancer resulted in a synergistic enhancement of transcription in the presence of GAL4. Furthermore, chimeras of the human estrogen receptor DNA binding domain and either GAL4 or GCN4 activating “acidic” regions can activate a promoter region controlled by an estrogen-responsive enhancer. Together, these data indicate that the molecular mechanisms responsible for transcriptional enhancement have been conserved from yeast to man.</p></abstract></profileDesc><revisionDesc><change when="1988">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-BW8F0VTZ-8/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier, elements deleted: tail"><istex:xmlDeclaration>version="1.0" encoding="utf-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//ES//DTD journal article DTD version 4.5.2//EN//XML" URI="art452.dtd" name="istex:docType"></istex:docType><istex:document><converted-article version="4.5.2" docsubtype="fla"><item-info><jid>CELL</jid><aid>88905053</aid><ce:pii>0092-8674(88)90505-3</ce:pii><ce:doi>10.1016/0092-8674(88)90505-3</ce:doi><ce:copyright type="unknown" year="1988"></ce:copyright></item-info><head><ce:dochead><ce:textfn>Article</ce:textfn></ce:dochead><ce:title>The yeast UAS<ce:inf>G</ce:inf> is a transcriptional enhancer in human hela cells in the presence of the GAL4 <ce:italic>trans</ce:italic>-activator</ce:title><ce:author-group><ce:author><ce:given-name>Nicholas</ce:given-name><ce:surname>Webster</ce:surname></ce:author><ce:author><ce:given-name>Jia Rui</ce:given-name><ce:surname>Jin</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>∗</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Stephen</ce:given-name><ce:surname>Green</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>∗</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Melvyn</ce:given-name><ce:surname>Hollis</ce:surname><ce:cross-ref refid="AFF2"><ce:sup>†</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Pierre</ce:given-name><ce:surname>Chambon</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>∗</ce:sup></ce:cross-ref></ce:author><ce:affiliation id="AFF1"><ce:label>a</ce:label><ce:textfn>Laboratoire de Génétique Moléculaire des Eucaryotes du CNRS Unité 184 de Biologie Moléculaire et de Génie Génétique de l'INSERM Institut de Chimie Biologique Faculté de Médecine 11, Rue Humann 67085 Strasbourg Cedex France</ce:textfn></ce:affiliation><ce:affiliation id="AFF2"><ce:label>b</ce:label><ce:textfn>Department of Biochemistry and Molecular Biology Harvard University Cambridge, Massachusetts 02138 USA</ce:textfn></ce:affiliation></ce:author-group><ce:date-received day="4" month="12" year="1987"></ce:date-received><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para>The yeast <ce:italic>trans</ce:italic>-activator protein GAL4, when expressed in HeLa cells, stimulates transcription from several class B (II) eukaryotic promoters containing GAL4 binding sites either as the full UAS<ce:inf>G</ce:inf> or as synthetic 17-mers. The characteristics of this activation are indistinguishable from those of the SV40 enhancer. Transcription was similarly stimulated from either complex promoter regions containing multiple upstream elements or from a simple promoter region composed of only a TATA box. Addition of a 17-mer GAL4 binding site to the SV40 enhancer resulted in a synergistic enhancement of transcription in the presence of GAL4. Furthermore, chimeras of the human estrogen receptor DNA binding domain and either GAL4 or GCN4 activating “acidic” regions can activate a promoter region controlled by an estrogen-responsive enhancer. Together, these data indicate that the molecular mechanisms responsible for transcriptional enhancement have been conserved from yeast to man.</ce:simple-para></ce:abstract-sec></ce:abstract></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>The yeast UASG is a transcriptional enhancer in human hela cells in the presence of the GAL4 trans -activator</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>The yeast UAS</title></titleInfo><name type="personal"><namePart type="given">Nicholas</namePart><namePart type="family">Webster</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jia Rui</namePart><namePart type="family">Jin</namePart><affiliation>Laboratoire de Génétique Moléculaire des Eucaryotes du CNRS Unité 184 de Biologie Moléculaire et de Génie Génétique de l'INSERM Institut de Chimie Biologique Faculté de Médecine 11, Rue Humann 67085 Strasbourg Cedex France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Stephen</namePart><namePart type="family">Green</namePart><affiliation>Laboratoire de Génétique Moléculaire des Eucaryotes du CNRS Unité 184 de Biologie Moléculaire et de Génie Génétique de l'INSERM Institut de Chimie Biologique Faculté de Médecine 11, Rue Humann 67085 Strasbourg Cedex France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Melvyn</namePart><namePart type="family">Hollis</namePart><affiliation>Department of Biochemistry and Molecular Biology Harvard University Cambridge, Massachusetts 02138 USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Pierre</namePart><namePart type="family">Chambon</namePart><affiliation>Laboratoire de Génétique Moléculaire des Eucaryotes du CNRS Unité 184 de Biologie Moléculaire et de Génie Génétique de l'INSERM Institut de Chimie Biologique Faculté de Médecine 11, Rue Humann 67085 Strasbourg Cedex France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="Full-length article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-1JC4F85T-7">research-article</genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1988</dateIssued><copyrightDate encoding="w3cdtf">1988</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><abstract lang="en">Abstract: The yeast trans-activator protein GAL4, when expressed in HeLa cells, stimulates transcription from several class B (II) eukaryotic promoters containing GAL4 binding sites either as the full UASG or as synthetic 17-mers. The characteristics of this activation are indistinguishable from those of the SV40 enhancer. Transcription was similarly stimulated from either complex promoter regions containing multiple upstream elements or from a simple promoter region composed of only a TATA box. Addition of a 17-mer GAL4 binding site to the SV40 enhancer resulted in a synergistic enhancement of transcription in the presence of GAL4. Furthermore, chimeras of the human estrogen receptor DNA binding domain and either GAL4 or GCN4 activating “acidic” regions can activate a promoter region controlled by an estrogen-responsive enhancer. Together, these data indicate that the molecular mechanisms responsible for transcriptional enhancement have been conserved from yeast to man.</abstract><note type="content">Section title: Article</note><relatedItem type="host"><titleInfo><title>Cell</title></titleInfo><titleInfo type="abbreviated"><title>CELL</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1988</dateIssued></originInfo><identifier type="ISSN">0092-8674</identifier><identifier type="PII">S0092-8674(00)X0420-5</identifier><part><date>1988</date><detail type="volume"><number>52</number><caption>vol.</caption></detail><detail type="issue"><number>2</number><caption>no.</caption></detail><extent unit="issue-pages"><start>153</start><end>301</end></extent><extent unit="pages"><start>169</start><end>178</end></extent></part></relatedItem><identifier type="istex">F93AD5F4E6BECF17113A3C523918F4C3B276E675</identifier><identifier type="ark">ark:/67375/6H6-BW8F0VTZ-8</identifier><identifier type="DOI">10.1016/0092-8674(88)90505-3</identifier><identifier type="PII">0092-8674(88)90505-3</identifier><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-HKKZVM7B-M">elsevier</recordContentSource></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/ark:/67375/6H6-BW8F0VTZ-8/record.json</uri></json:item></metadata></istex></record>Pour manipuler ce document sous Unix (Dilib)
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