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Article: Binding sites for transcription factor NTF-1/Elf-1 contribute to the ventral repression of decapentaplegic

TitleBinding sites for transcription factor NTF-1/Elf-1 contribute to the ventral repression of decapentaplegic
Authors
Keywordscorepressor
Decapentaplegic
dorsal morphogen
dorsal/ventral pattern formation
transcription
Issue Date1995
PublisherCold Spring Harbor Laboratory Press. The Journal's web site is located at http://genesdev.cshlp.org/
Citation
Genes And Development, 1995, v. 9 n. 24, p. 3177-3189 How to Cite?
AbstractThe Dorsal morphogen is a transcription factor that activates some genes and represses others to establish multiple domains of gene expression along the dorsal/ventral axis of the early Drosophila embryo. Repression by Dorsal appears to require accessory proteins that bind to corepression elements in Dorsal-dependent regulatory modules called ventral repression regions (VRRs). We have identified a corepression element in decapentaplegic (dpp), a zygotically active gene that is repressed by the Dorsal morphogen. This dpp repression element (DRE) is located within a previously identified VRR and close to essential Dorsal-binding sites. We have purified a factor from Drosophila embryo extracts that binds to the DRE but not to mutant forms of the DRE that fail to support efficient repression. This protein also binds to an apparently essential region in a VRR associated with the zerknullt (zen) gene. One of the DREs in the dpp VRR overlaps the binding site for a potential activator protein suggesting that one mechanism of ventral repression may be the mutually exclusive binding of repressor and activator proteins. We have found the DRE-binding protein to be identical to NTF-1 (equivalent to Elf-1, the product of the grainyhead gene), a factor originally identified as an activator of the Ultrabithorax and Dopa decarboxylase promoters. NTF-1 mRNA is synthesized during oogenesis and deposited in the developing oocyte where it is available to contribute to ventral repression during early embryogenesis. Previous studies have shown that overexpression of NTF-1 in the postblastoderm embryo results in a phenotype that is consistent with a role for this factor in the repression of dpp later in embryogenesis.
Persistent Identifierhttp://hdl.handle.net/10722/147401
ISSN
2021 Impact Factor: 12.890
2020 SCImago Journal Rankings: 7.136
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorHuang, JDen_US
dc.contributor.authorDubnicoff, Ten_US
dc.contributor.authorLiaw, GJen_US
dc.contributor.authorBai, Yen_US
dc.contributor.authorValentine, SAen_US
dc.contributor.authorShirokawa, JMen_US
dc.contributor.authorLengyel, JAen_US
dc.contributor.authorCourey, AJen_US
dc.date.accessioned2012-05-29T06:03:28Z-
dc.date.available2012-05-29T06:03:28Z-
dc.date.issued1995en_US
dc.identifier.citationGenes And Development, 1995, v. 9 n. 24, p. 3177-3189en_US
dc.identifier.issn0890-9369en_US
dc.identifier.urihttp://hdl.handle.net/10722/147401-
dc.description.abstractThe Dorsal morphogen is a transcription factor that activates some genes and represses others to establish multiple domains of gene expression along the dorsal/ventral axis of the early Drosophila embryo. Repression by Dorsal appears to require accessory proteins that bind to corepression elements in Dorsal-dependent regulatory modules called ventral repression regions (VRRs). We have identified a corepression element in decapentaplegic (dpp), a zygotically active gene that is repressed by the Dorsal morphogen. This dpp repression element (DRE) is located within a previously identified VRR and close to essential Dorsal-binding sites. We have purified a factor from Drosophila embryo extracts that binds to the DRE but not to mutant forms of the DRE that fail to support efficient repression. This protein also binds to an apparently essential region in a VRR associated with the zerknullt (zen) gene. One of the DREs in the dpp VRR overlaps the binding site for a potential activator protein suggesting that one mechanism of ventral repression may be the mutually exclusive binding of repressor and activator proteins. We have found the DRE-binding protein to be identical to NTF-1 (equivalent to Elf-1, the product of the grainyhead gene), a factor originally identified as an activator of the Ultrabithorax and Dopa decarboxylase promoters. NTF-1 mRNA is synthesized during oogenesis and deposited in the developing oocyte where it is available to contribute to ventral repression during early embryogenesis. Previous studies have shown that overexpression of NTF-1 in the postblastoderm embryo results in a phenotype that is consistent with a role for this factor in the repression of dpp later in embryogenesis.en_US
dc.languageengen_US
dc.publisherCold Spring Harbor Laboratory Press. The Journal's web site is located at http://genesdev.cshlp.org/en_US
dc.relation.ispartofGenes and Developmenten_US
dc.subjectcorepressor-
dc.subjectDecapentaplegic-
dc.subjectdorsal morphogen-
dc.subjectdorsal/ventral pattern formation-
dc.subjecttranscription-
dc.subject.meshAnimalsen_US
dc.subject.meshBase Sequenceen_US
dc.subject.meshBinding Sitesen_US
dc.subject.meshDnaen_US
dc.subject.meshDna-Binding Proteins - Metabolismen_US
dc.subject.meshDrosophila - Embryology - Geneticsen_US
dc.subject.meshDrosophila Proteinsen_US
dc.subject.meshFemaleen_US
dc.subject.meshGenomic Imprintingen_US
dc.subject.meshInsect Hormones - Geneticsen_US
dc.subject.meshMolecular Sequence Dataen_US
dc.subject.meshPoint Mutationen_US
dc.subject.meshSuppression, Geneticen_US
dc.subject.meshTranscription Factors - Metabolismen_US
dc.subject.meshTransforming Growth Factor Beta - Geneticsen_US
dc.titleBinding sites for transcription factor NTF-1/Elf-1 contribute to the ventral repression of decapentaplegicen_US
dc.typeArticleen_US
dc.identifier.emailHuang, JD:jdhuang@hkucc.hku.hken_US
dc.identifier.authorityHuang, JD=rp00451en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1101/gad.9.24.3177-
dc.identifier.pmid8543160-
dc.identifier.scopuseid_2-s2.0-0029592140en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0029592140&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume9en_US
dc.identifier.issue24en_US
dc.identifier.spage3177en_US
dc.identifier.epage3189en_US
dc.identifier.isiWOS:A1995TM48000012-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridHuang, JD=8108660600en_US
dc.identifier.scopusauthoridDubnicoff, T=6506930007en_US
dc.identifier.scopusauthoridLiaw, GJ=7004548643en_US
dc.identifier.scopusauthoridBai, Y=7402572209en_US
dc.identifier.scopusauthoridValentine, SA=35886692300en_US
dc.identifier.scopusauthoridShirokawa, JM=6602300857en_US
dc.identifier.scopusauthoridLengyel, JA=7005785362en_US
dc.identifier.scopusauthoridCourey, AJ=7003350876en_US
dc.identifier.issnl0890-9369-

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