File Download
  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Auto/cross-regulation of Hoxb3 expression in posterior hindbrain and spinal cord

TitleAuto/cross-regulation of Hoxb3 expression in posterior hindbrain and spinal cord
Authors
Issue Date2002
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/ydbio
Citation
Developmental Biology, 2002, v. 252 n. 2, p. 287-300 How to Cite?
AbstractThe complex and dynamic pattern of Hoxb3 expression in the developing hindbrain and the associated neural crest of mouse embryos is controlled by three separate cis-regulatory elements: element I (region A), element IIIa, and the r5 enhancer (element IVa). We have examined the cis-regulatory element IIIa by transgenic and mutational analysis to determine the upstream trans-acting factors and mechanisms that are involved in controlling the expression of the mouse Hoxb3 gene in the anterior spinal cord and hindbrain up to the r5/r6 boundary, as well as the associated neural crest which migrate to the third and posterior branchial arches and to the gut. By deletion analysis, we have identified the sequence requirements within a 482-bp element III482. Two Hox binding sites are identified in element III482 and we have shown that in vitro both Hoxb3 and Hoxb4 proteins can interact with these Hox binding sites, suggesting that auto/cross-regulation is required for establishing the expression of Hoxb3 in the neural tube domain. Interestingly, we have identified a novel GCCAGGC sequence motif within element III482, which is also required to direct gene expression to a subset of the expression domains except for rhombomere 6 and the associated neural crest migrating to the third and posterior branchial arches. Element III482 can direct a higher level of reporter gene expression in r6, which led us to investigate whether kreisler is involved in regulating Hoxb3 expression in r6 through this element. However, our transgenic and mutational analysis has demonstrated that, although kreisler binding sites are present, they are not required for the establishment or maintenance of reporter gene expression in r6. Our results have provided evidence that the expression of Hoxb3 in the neural tube up to the r5/r6 boundary is auto/cross-regulated by Hox genes and expression of Hoxb3 in r6 does not require kreisler. © 2002 Elsevier Science (USA).
Persistent Identifierhttp://hdl.handle.net/10722/68314
ISSN
2015 Impact Factor: 3.155
2015 SCImago Journal Rankings: 2.554
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorYau, TOen_HK
dc.contributor.authorKwan, CTen_HK
dc.contributor.authorJakt, LMen_HK
dc.contributor.authorStallwood, Nen_HK
dc.contributor.authorCordes, Sen_HK
dc.contributor.authorSham, MHen_HK
dc.date.accessioned2010-09-06T06:03:24Z-
dc.date.available2010-09-06T06:03:24Z-
dc.date.issued2002en_HK
dc.identifier.citationDevelopmental Biology, 2002, v. 252 n. 2, p. 287-300en_HK
dc.identifier.issn0012-1606en_HK
dc.identifier.urihttp://hdl.handle.net/10722/68314-
dc.description.abstractThe complex and dynamic pattern of Hoxb3 expression in the developing hindbrain and the associated neural crest of mouse embryos is controlled by three separate cis-regulatory elements: element I (region A), element IIIa, and the r5 enhancer (element IVa). We have examined the cis-regulatory element IIIa by transgenic and mutational analysis to determine the upstream trans-acting factors and mechanisms that are involved in controlling the expression of the mouse Hoxb3 gene in the anterior spinal cord and hindbrain up to the r5/r6 boundary, as well as the associated neural crest which migrate to the third and posterior branchial arches and to the gut. By deletion analysis, we have identified the sequence requirements within a 482-bp element III482. Two Hox binding sites are identified in element III482 and we have shown that in vitro both Hoxb3 and Hoxb4 proteins can interact with these Hox binding sites, suggesting that auto/cross-regulation is required for establishing the expression of Hoxb3 in the neural tube domain. Interestingly, we have identified a novel GCCAGGC sequence motif within element III482, which is also required to direct gene expression to a subset of the expression domains except for rhombomere 6 and the associated neural crest migrating to the third and posterior branchial arches. Element III482 can direct a higher level of reporter gene expression in r6, which led us to investigate whether kreisler is involved in regulating Hoxb3 expression in r6 through this element. However, our transgenic and mutational analysis has demonstrated that, although kreisler binding sites are present, they are not required for the establishment or maintenance of reporter gene expression in r6. Our results have provided evidence that the expression of Hoxb3 in the neural tube up to the r5/r6 boundary is auto/cross-regulated by Hox genes and expression of Hoxb3 in r6 does not require kreisler. © 2002 Elsevier Science (USA).en_HK
dc.languageengen_HK
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/ydbioen_HK
dc.relation.ispartofDevelopmental Biologyen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subject.meshAnimalsen_HK
dc.subject.meshBase Sequenceen_HK
dc.subject.meshBinding Sitesen_HK
dc.subject.meshDNAen_HK
dc.subject.meshElectrophoretic Mobility Shift Assayen_HK
dc.subject.meshEnhancer Elements, Geneticen_HK
dc.subject.meshGene Expression Regulation, Developmentalen_HK
dc.subject.meshGenes, Homeoboxen_HK
dc.subject.meshMiceen_HK
dc.subject.meshMice, Transgenicen_HK
dc.subject.meshMolecular Sequence Dataen_HK
dc.subject.meshRhombencephalon - metabolismen_HK
dc.subject.meshSpinal Cord - metabolismen_HK
dc.titleAuto/cross-regulation of Hoxb3 expression in posterior hindbrain and spinal corden_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0012-1606&volume=252&spage=287&epage=300&date=2002&atitle=Auto/Cross-regulation+of+Hoxb3+expression+in+posterior+hindbrain+and+spinal+corden_HK
dc.identifier.emailSham, MH:mhsham@hkucc.hku.hken_HK
dc.identifier.authoritySham, MH=rp00380en_HK
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1006/dbio.2002.0849en_HK
dc.identifier.pmid12482716-
dc.identifier.scopuseid_2-s2.0-0036933316en_HK
dc.identifier.hkuros84085en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0036933316&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume252en_HK
dc.identifier.issue2en_HK
dc.identifier.spage287en_HK
dc.identifier.epage300en_HK
dc.identifier.isiWOS:000180122800010-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridYau, TO=7006540669en_HK
dc.identifier.scopusauthoridKwan, CT=7201421142en_HK
dc.identifier.scopusauthoridJakt, LM=6507406360en_HK
dc.identifier.scopusauthoridStallwood, N=6507309202en_HK
dc.identifier.scopusauthoridCordes, S=7005622768en_HK
dc.identifier.scopusauthoridSham, MH=7003729109en_HK

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats