Ecdysterone regulatory elements function as both transcriptional activators and repressors.
Identifieur interne : 002A01 ( PubMed/Corpus ); précédent : 002A00; suivant : 002A02Ecdysterone regulatory elements function as both transcriptional activators and repressors.
Auteurs : L. Dobens ; K. Rudolph ; E M BergerSource :
- Molecular and cellular biology [ 0270-7306 ] ; 1991.
English descriptors
- KwdEn :
- Animals, Base Sequence, Binding, Competitive, Cells, Cultured, Cloning, Molecular, Drosophila (genetics), Ecdysterone (genetics), Ecdysterone (pharmacology), Gene Expression Regulation, Heat-Shock Proteins (genetics), Molecular Sequence Data, Promoter Regions, Genetic, Regulatory Sequences, Nucleic Acid, Transcription Factors (genetics), Transcription Factors (metabolism), Transcription, Genetic, Transfection.
- MESH :
- chemical , genetics : Ecdysterone, Heat-Shock Proteins, Transcription Factors.
- genetics : Drosophila.
- chemical , metabolism : Transcription Factors.
- chemical , pharmacology : Ecdysterone.
- Animals, Base Sequence, Binding, Competitive, Cells, Cultured, Cloning, Molecular, Gene Expression Regulation, Molecular Sequence Data, Promoter Regions, Genetic, Regulatory Sequences, Nucleic Acid, Transcription, Genetic, Transfection.
Abstract
A synthetic, 23-bp ecdysterone regulatory element (EcRE), derived from the upstream region of the Drosophila melanogaster hsp27 gene, was inserted adjacent to the herpes simplex virus thymidine kinase promoter fused to a bacterial gene for chloramphenicol acetyltransferase (CAT). Hybrid constructs were transfected into Drosophila S3 cells and assayed for ecdysterone-inducible CAT expression. In the absence of ecdysterone a tandem pair of EcREs repressed the high constitutive level of CAT activity found after transfection with the parent reporter plasmid alone. After hormone addition very high levels of CAT activity were observed. Insertion of the EcRE pair 3' of the CAT gene also led to high levels of ecdysterone-induced CAT expression, but the repression of high constitutive levels of CAT activity failed to occur. The EcRE-CAT construct was cotransfected with plasmids containing tandem 10-mers or 40-mers of the EcRE but lacking a reporter gene. These additional EcREs led to a reduced level of ecdysterone-induced CAT activity and to an elevation of basal CAT activity in the absence of hormone. The data suggest that the receptor binds to the EcRE in the absence of hormone, blocking basal transcription from a constitutive promoter. In the presence of ecdysterone, receptor-hormone binding to the EcRE leads to greatly enhanced transcription.
DOI: 10.1128/mcb.11.4.1846
PubMed: 2005885
Links to Exploration step
pubmed:2005885Le document en format XML
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Rudolph</name></author><author><name sortKey="Berger, E M" sort="Berger, E M" uniqKey="Berger E" first="E M" last="Berger">E M Berger</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1991">1991</date><idno type="RBID">pubmed:2005885</idno><idno type="pmid">2005885</idno><idno type="doi">10.1128/mcb.11.4.1846</idno><idno type="wicri:Area/PubMed/Corpus">002A01</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">002A01</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Ecdysterone regulatory elements function as both transcriptional activators and repressors.</title><author><name sortKey="Dobens, L" sort="Dobens, L" uniqKey="Dobens L" first="L" last="Dobens">L. Dobens</name><affiliation><nlm:affiliation>Department of Biological Sciences, Dartmouth College, Hanover, New Hampshire 03755.</nlm:affiliation></affiliation></author><author><name sortKey="Rudolph, K" sort="Rudolph, K" uniqKey="Rudolph K" first="K" last="Rudolph">K. Rudolph</name></author><author><name sortKey="Berger, E M" sort="Berger, E M" uniqKey="Berger E" first="E M" last="Berger">E M Berger</name></author></analytic><series><title level="j">Molecular and cellular biology</title><idno type="ISSN">0270-7306</idno><imprint><date when="1991" type="published">1991</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Base Sequence</term><term>Binding, Competitive</term><term>Cells, Cultured</term><term>Cloning, Molecular</term><term>Drosophila (genetics)</term><term>Ecdysterone (genetics)</term><term>Ecdysterone (pharmacology)</term><term>Gene Expression Regulation</term><term>Heat-Shock Proteins (genetics)</term><term>Molecular Sequence Data</term><term>Promoter Regions, Genetic</term><term>Regulatory Sequences, Nucleic Acid</term><term>Transcription Factors (genetics)</term><term>Transcription Factors (metabolism)</term><term>Transcription, Genetic</term><term>Transfection</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Ecdysterone</term><term>Heat-Shock Proteins</term><term>Transcription Factors</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Drosophila</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Transcription Factors</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Ecdysterone</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Base Sequence</term><term>Binding, Competitive</term><term>Cells, Cultured</term><term>Cloning, Molecular</term><term>Gene Expression Regulation</term><term>Molecular Sequence Data</term><term>Promoter Regions, Genetic</term><term>Regulatory Sequences, Nucleic Acid</term><term>Transcription, Genetic</term><term>Transfection</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">A synthetic, 23-bp ecdysterone regulatory element (EcRE), derived from the upstream region of the Drosophila melanogaster hsp27 gene, was inserted adjacent to the herpes simplex virus thymidine kinase promoter fused to a bacterial gene for chloramphenicol acetyltransferase (CAT). Hybrid constructs were transfected into Drosophila S3 cells and assayed for ecdysterone-inducible CAT expression. In the absence of ecdysterone a tandem pair of EcREs repressed the high constitutive level of CAT activity found after transfection with the parent reporter plasmid alone. After hormone addition very high levels of CAT activity were observed. Insertion of the EcRE pair 3' of the CAT gene also led to high levels of ecdysterone-induced CAT expression, but the repression of high constitutive levels of CAT activity failed to occur. The EcRE-CAT construct was cotransfected with plasmids containing tandem 10-mers or 40-mers of the EcRE but lacking a reporter gene. These additional EcREs led to a reduced level of ecdysterone-induced CAT activity and to an elevation of basal CAT activity in the absence of hormone. The data suggest that the receptor binds to the EcRE in the absence of hormone, blocking basal transcription from a constitutive promoter. In the presence of ecdysterone, receptor-hormone binding to the EcRE leads to greatly enhanced transcription.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">2005885</PMID><DateCompleted><Year>1991</Year><Month>04</Month><Day>22</Day></DateCompleted><DateRevised><Year>2019</Year><Month>05</Month><Day>08</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0270-7306</ISSN><JournalIssue CitedMedium="Print"><Volume>11</Volume><Issue>4</Issue><PubDate><Year>1991</Year><Month>Apr</Month></PubDate></JournalIssue><Title>Molecular and cellular biology</Title><ISOAbbreviation>Mol. Cell. Biol.</ISOAbbreviation></Journal><ArticleTitle>Ecdysterone regulatory elements function as both transcriptional activators and repressors.</ArticleTitle><Pagination><MedlinePgn>1846-53</MedlinePgn></Pagination><Abstract><AbstractText>A synthetic, 23-bp ecdysterone regulatory element (EcRE), derived from the upstream region of the Drosophila melanogaster hsp27 gene, was inserted adjacent to the herpes simplex virus thymidine kinase promoter fused to a bacterial gene for chloramphenicol acetyltransferase (CAT). Hybrid constructs were transfected into Drosophila S3 cells and assayed for ecdysterone-inducible CAT expression. In the absence of ecdysterone a tandem pair of EcREs repressed the high constitutive level of CAT activity found after transfection with the parent reporter plasmid alone. After hormone addition very high levels of CAT activity were observed. Insertion of the EcRE pair 3' of the CAT gene also led to high levels of ecdysterone-induced CAT expression, but the repression of high constitutive levels of CAT activity failed to occur. The EcRE-CAT construct was cotransfected with plasmids containing tandem 10-mers or 40-mers of the EcRE but lacking a reporter gene. These additional EcREs led to a reduced level of ecdysterone-induced CAT activity and to an elevation of basal CAT activity in the absence of hormone. The data suggest that the receptor binds to the EcRE in the absence of hormone, blocking basal transcription from a constitutive promoter. In the presence of ecdysterone, receptor-hormone binding to the EcRE leads to greatly enhanced transcription.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Dobens</LastName><ForeName>L</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Department of Biological Sciences, Dartmouth College, Hanover, New Hampshire 03755.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rudolph</LastName><ForeName>K</ForeName><Initials>K</Initials></Author><Author ValidYN="Y"><LastName>Berger</LastName><ForeName>E M</ForeName><Initials>EM</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</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></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="D006360">Heat-Shock Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D014157">Transcription Factors</NameOfSubstance></Chemical><Chemical><RegistryNumber>5289-74-7</RegistryNumber><NameOfSubstance UI="D004441">Ecdysterone</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><GeneSymbolList><GeneSymbol>hsp27</GeneSymbol></GeneSymbolList><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001483" MajorTopicYN="N">Base Sequence</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001667" MajorTopicYN="N">Binding, Competitive</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002478" MajorTopicYN="N">Cells, Cultured</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003001" MajorTopicYN="N">Cloning, Molecular</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004330" MajorTopicYN="N">Drosophila</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004441" MajorTopicYN="N">Ecdysterone</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005786" MajorTopicYN="Y">Gene Expression Regulation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006360" MajorTopicYN="N">Heat-Shock Proteins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008969" MajorTopicYN="N">Molecular Sequence Data</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011401" MajorTopicYN="N">Promoter Regions, Genetic</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D012045" MajorTopicYN="Y">Regulatory Sequences, Nucleic Acid</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><MeshHeading><DescriptorName UI="D014158" MajorTopicYN="Y">Transcription, Genetic</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014162" MajorTopicYN="N">Transfection</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1991</Year><Month>4</Month><Day>1</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1991</Year><Month>4</Month><Day>1</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate 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