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Article: The torso response element binds GAGA and NTF-1/Elf-1, and regulates tailless by relief of repression

TitleThe torso response element binds GAGA and NTF-1/Elf-1, and regulates tailless by relief of repression
Authors
KeywordsElf- 1
GAGA
grainyhead
NTF-1
tailless
Torso tyrosine kinase receptor
transcription factor
Trithorax-like
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. 3163-3176 How to Cite?
AbstractModulation of transcription factor activity leading to changes in cell behavior (e.g., differentiation versus proliferation) is one of the critical outcomes of receptor tyrosine kinase (RTK) stimulation. In the early Drosophila embryo, activation of the torso (tor) RTK at the poles of the embryo activates a phosphorylation cascade that leads to the spatially specific transcription of the tailless (tll) gene. Our analysis of the tor response element (tor-RE) in the tll promoter indicates that the key activity modulated by the tor RTK pathway is a repressor present throughout the embryo. We have mapped the tor-RE to an 11-bp sequence; using this sequence as the basis for protein purification, we have determined that the proteins GAGA and NTF-1 (also known as Elf-1, product of the grainyhead gene) bind to the tor-RE. We demonstrate that NTF-1 can be phosphorylated by MAPK (mitogen- activated protein kinase), and that tll expression is expanded in embryos lacking maternal NTF-1 activity; these results make NTF-1 a likely target for modulation by the tor RTK pathway in vivo. The data presented here support a model in which activation of the tor RTK at the poles of the embryos leads to inactivation of the repressor and therefore, to transcriptional activation (by activators present throughout the embryo) of the tll gene at the poles of the embryo.
Persistent Identifierhttp://hdl.handle.net/10722/147402
ISSN
2023 Impact Factor: 7.5
2023 SCImago Journal Rankings: 5.015
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLiaw, GJen_US
dc.contributor.authorRudolph, KMen_US
dc.contributor.authorHuang, JDen_US
dc.contributor.authorDubnicoff, Ten_US
dc.contributor.authorCourey, AJen_US
dc.contributor.authorLengyel, JAen_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. 3163-3176en_US
dc.identifier.issn0890-9369en_US
dc.identifier.urihttp://hdl.handle.net/10722/147402-
dc.description.abstractModulation of transcription factor activity leading to changes in cell behavior (e.g., differentiation versus proliferation) is one of the critical outcomes of receptor tyrosine kinase (RTK) stimulation. In the early Drosophila embryo, activation of the torso (tor) RTK at the poles of the embryo activates a phosphorylation cascade that leads to the spatially specific transcription of the tailless (tll) gene. Our analysis of the tor response element (tor-RE) in the tll promoter indicates that the key activity modulated by the tor RTK pathway is a repressor present throughout the embryo. We have mapped the tor-RE to an 11-bp sequence; using this sequence as the basis for protein purification, we have determined that the proteins GAGA and NTF-1 (also known as Elf-1, product of the grainyhead gene) bind to the tor-RE. We demonstrate that NTF-1 can be phosphorylated by MAPK (mitogen- activated protein kinase), and that tll expression is expanded in embryos lacking maternal NTF-1 activity; these results make NTF-1 a likely target for modulation by the tor RTK pathway in vivo. The data presented here support a model in which activation of the tor RTK at the poles of the embryos leads to inactivation of the repressor and therefore, to transcriptional activation (by activators present throughout the embryo) of the tll gene at the poles of the embryo.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.subjectElf- 1-
dc.subjectGAGA-
dc.subjectgrainyhead-
dc.subjectNTF-1-
dc.subjecttailless-
dc.subjectTorso tyrosine kinase receptor-
dc.subjecttranscription factor-
dc.subjectTrithorax-like-
dc.subject.meshAnimalsen_US
dc.subject.meshBase Sequenceen_US
dc.subject.meshDnaen_US
dc.subject.meshDna-Binding Proteins - Genetics - Metabolismen_US
dc.subject.meshDrosophila - Embryology - Geneticsen_US
dc.subject.meshDrosophila Proteinsen_US
dc.subject.meshGene Expression Regulation, Developmentalen_US
dc.subject.meshHomeodomain Proteins - Metabolismen_US
dc.subject.meshMolecular Sequence Dataen_US
dc.subject.meshPromoter Regions, Geneticen_US
dc.subject.meshProtein-Tyrosine Kinases - Metabolismen_US
dc.subject.meshReceptor Protein-Tyrosine Kinasesen_US
dc.subject.meshRepressor Proteins - Geneticsen_US
dc.subject.meshSuppression, Geneticen_US
dc.subject.meshTranscription Factors - Metabolismen_US
dc.titleThe torso response element binds GAGA and NTF-1/Elf-1, and regulates tailless by relief of repressionen_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.9.24.3163-
dc.identifier.pmid8543159en_US
dc.identifier.scopuseid_2-s2.0-0029595272en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0029595272&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume9en_US
dc.identifier.issue24en_US
dc.identifier.spage3163en_US
dc.identifier.epage3176en_US
dc.identifier.isiWOS:A1995TM48000011-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridLiaw, GJ=7004548643en_US
dc.identifier.scopusauthoridRudolph, KM=7103298253en_US
dc.identifier.scopusauthoridHuang, JD=8108660600en_US
dc.identifier.scopusauthoridDubnicoff, T=6506930007en_US
dc.identifier.scopusauthoridCourey, AJ=7003350876en_US
dc.identifier.scopusauthoridLengyel, JA=7005785362en_US
dc.identifier.issnl0890-9369-

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