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Article: Cross-regulation in the mouse HoxB complex: The expression of Hoxb2 in rhombomere 4 is regulated by Hoxb1

TitleCross-regulation in the mouse HoxB complex: The expression of Hoxb2 in rhombomere 4 is regulated by Hoxb1
Authors
Issue Date1997
PublisherCold Spring Harbor Laboratory Press. The Journal's web site is located at http://genesdev.cshlp.org/
Citation
Genes And Development, 1997, v. 11 n. 14, p. 1885-1895 How to Cite?
AbstractCorrect regulation of the segment-restricted patterns of Hox gene expression is essential for proper patterning of the vertebrate hindbrain. We have examined the molecular basis of restricted expression of Hoxb2 in rhombomere 4 (r4), by using deletion analysis in transgenic mice to identify an r4 enhancer from the mouse gene. A bipartite Hox/Pbx binding motif is located within this enhancer, and in vitro DNA binding experiments showed that the vertebrate labial-related protein Hoxb1 will cooperatively bind to this site in a Pbx/Exd-dependent manner. The Hoxb2 r4 enhancer can be transactivated in vivo by the ectopic expression of Hoxb1, Hoxa1, and Drosophila labial in transgenic mice. In contrast, ectopic Hoxb2 and Hoxb4 are unable to induce expression, indicating that in vivo this enhancer preferentially responds to labial family members. Mutational analysis demonstrated that the bipartite Hox/Pbx motif is required for r4 enhancer activity and the responses to retinoids and ectopic Hox expression. Furthermore, three copies of the Hoxb2 motif are sufficient to mediate r4 expression in transgenic mouse embryos and a labial pattern in Drosophila embryos. This reporter expression in Drosophila embryos is dependent upon endogenous labial and exd, suggesting that the ability of this Hox/Pbx site to interact with labial-related proteins has been evolutionarily conserved. The endogenous Hoxb2 gene is no longer upregulated in r4 in Hoxb1 homozygous mutant embryos. On the basis of these experiments we conclude that the r4- restricted domain of Hoxb2 in the hindbrain is the result of a direct cross- regulatory interaction by Hoxb1 involving vertebrate Pbx proteins as cofactors. This suggests that part of the functional role of Hoxb1 in maintaining r4 identity may be mediated by the Hoxb2 gene.
Persistent Identifierhttp://hdl.handle.net/10722/68158
ISSN
2015 Impact Factor: 10.042
2015 SCImago Journal Rankings: 11.812
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorMaconochie, MKen_HK
dc.contributor.authorNonchev, Sen_HK
dc.contributor.authorStuder, Men_HK
dc.contributor.authorChan, SKen_HK
dc.contributor.authorPöpperl, Hen_HK
dc.contributor.authorSham, MHen_HK
dc.contributor.authorMann, RSen_HK
dc.contributor.authorKrumlauf, Ren_HK
dc.date.accessioned2010-09-06T06:01:55Z-
dc.date.available2010-09-06T06:01:55Z-
dc.date.issued1997en_HK
dc.identifier.citationGenes And Development, 1997, v. 11 n. 14, p. 1885-1895en_HK
dc.identifier.issn0890-9369en_HK
dc.identifier.urihttp://hdl.handle.net/10722/68158-
dc.description.abstractCorrect regulation of the segment-restricted patterns of Hox gene expression is essential for proper patterning of the vertebrate hindbrain. We have examined the molecular basis of restricted expression of Hoxb2 in rhombomere 4 (r4), by using deletion analysis in transgenic mice to identify an r4 enhancer from the mouse gene. A bipartite Hox/Pbx binding motif is located within this enhancer, and in vitro DNA binding experiments showed that the vertebrate labial-related protein Hoxb1 will cooperatively bind to this site in a Pbx/Exd-dependent manner. The Hoxb2 r4 enhancer can be transactivated in vivo by the ectopic expression of Hoxb1, Hoxa1, and Drosophila labial in transgenic mice. In contrast, ectopic Hoxb2 and Hoxb4 are unable to induce expression, indicating that in vivo this enhancer preferentially responds to labial family members. Mutational analysis demonstrated that the bipartite Hox/Pbx motif is required for r4 enhancer activity and the responses to retinoids and ectopic Hox expression. Furthermore, three copies of the Hoxb2 motif are sufficient to mediate r4 expression in transgenic mouse embryos and a labial pattern in Drosophila embryos. This reporter expression in Drosophila embryos is dependent upon endogenous labial and exd, suggesting that the ability of this Hox/Pbx site to interact with labial-related proteins has been evolutionarily conserved. The endogenous Hoxb2 gene is no longer upregulated in r4 in Hoxb1 homozygous mutant embryos. On the basis of these experiments we conclude that the r4- restricted domain of Hoxb2 in the hindbrain is the result of a direct cross- regulatory interaction by Hoxb1 involving vertebrate Pbx proteins as cofactors. This suggests that part of the functional role of Hoxb1 in maintaining r4 identity may be mediated by the Hoxb2 gene.en_HK
dc.languageengen_HK
dc.publisherCold Spring Harbor Laboratory Press. The Journal's web site is located at http://genesdev.cshlp.org/en_HK
dc.relation.ispartofGenes and Developmenten_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshBase Sequenceen_HK
dc.subject.meshDrosophila - embryology - geneticsen_HK
dc.subject.meshEnhancer Elements, Geneticen_HK
dc.subject.meshGene Expression Regulation, Developmentalen_HK
dc.subject.meshHomeodomain Proteins - genetics - metabolismen_HK
dc.subject.meshMiceen_HK
dc.subject.meshMice, Inbred C57BLen_HK
dc.subject.meshMice, Inbred CBAen_HK
dc.subject.meshMice, Transgenicen_HK
dc.subject.meshMolecular Sequence Dataen_HK
dc.subject.meshProtein Bindingen_HK
dc.subject.meshTranscription Factors - genetics - metabolismen_HK
dc.subject.meshTranscriptional Activationen_HK
dc.titleCross-regulation in the mouse HoxB complex: The expression of Hoxb2 in rhombomere 4 is regulated by Hoxb1en_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0890-9369&volume=11&spage=1885&epage=1895&date=1997&atitle=Cross-regulation+in+the+mouse+HoxB+complex:+the+expression+of+Hoxb2+in+rhombomere+4+is+regulated+by+Hoxb1en_HK
dc.identifier.emailSham, MH:mhsham@hkucc.hku.hken_HK
dc.identifier.authoritySham, MH=rp00380en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.pmid9242495-
dc.identifier.scopuseid_2-s2.0-0030746837en_HK
dc.identifier.hkuros36629en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0030746837&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume11en_HK
dc.identifier.issue14en_HK
dc.identifier.spage1885en_HK
dc.identifier.epage1895en_HK
dc.identifier.isiWOS:A1997XM83500011-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridMaconochie, MK=6603785710en_HK
dc.identifier.scopusauthoridNonchev, S=6603818489en_HK
dc.identifier.scopusauthoridStuder, M=7005938648en_HK
dc.identifier.scopusauthoridChan, SK=7404255792en_HK
dc.identifier.scopusauthoridPöpperl, H=6701474389en_HK
dc.identifier.scopusauthoridSham, MH=7003729109en_HK
dc.identifier.scopusauthoridMann, RS=7401908142en_HK
dc.identifier.scopusauthoridKrumlauf, R=8874137700en_HK

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