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Conference Paper: Over-expression of mutant SOX10 in the vagal neural crest causes hypoganglionic colon development in transgenic mice

TitleOver-expression of mutant SOX10 in the vagal neural crest causes hypoganglionic colon development in transgenic mice
Authors
Issue Date2003
PublisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/NMO
Citation
The 2003 International Conference on Enteric Nervous System, Banff, AB., Canada 9-13 July 2003. In Neurogastroenterology and Motility, 2003, v. 15 n. 2, p. 200, abstract no. 16 How to Cite?
AbstractThe neural and glial cells of the intrinsic ganglia of the enteric nervous system (ENS) are derived from the hindbrain neural crest at the vagal level (VNC), but the sacral neural crest (SNC) also has some contribution. The coordination of neural crest migration and the molecular control of their differentiation into specific cell types are not clearly known. Several genes have been found to be involved in ENS development, including Sox10 which when mutated caused megacolon in mice as observed in the Dom mutant. We have identified a VNC specific enhancer element from the mouse Hoxb3 gene, b3-IIIa, which could direct lacZ reporter gene expression in the ENS of transgenic mice. When crossed with the Dom mutant, the hybrid mutant displayed an absence of lacZ marked cells in the hindgut, further con- firming the specificity of this enhancer in the ENS. In order to understand the role of Sox10 during the development of vagal neural crest to the ENS, we have taken a transgenic approach making use of the VNC specific enhancer. We have generated a gain-of-function mutant in which mutant Sox10 with a Dom mutation was ectopically expressed in the vagal neural crest of transgenic mice. The mutants did not have a megacolon phenotype, but immunohistochemical analysis of 14.5 and 16.5 dpc transgenic mutant embryos using anti-neurofilament antibody showed that the ENS development was affected. The distal colons of the mutants were hypoganglionic, with deficient number and complexity of ganglionic plexuses. It is possible that in the transgenic mice, the mutant Sox10 proteins expressed in the VNC may compete with wildtype proteins in a dominant negative manner and as a consequence affect the proliferation and/or differentiation of the enteric ganglia.
Descriptionpp. 195–237 of this journal issue entitled: Abstracts presented at ENTERIC NERVOUS SYSTEM 2003 An international conference devoted to studies of the enteric nervous system ... 2003
Persistent Identifierhttp://hdl.handle.net/10722/96385
ISSN
2015 Impact Factor: 3.31
2015 SCImago Journal Rankings: 1.722

 

DC FieldValueLanguage
dc.contributor.authorSham, MHen_HK
dc.contributor.authorChan, KKen_HK
dc.contributor.authorChen, AYSen_HK
dc.contributor.authorLui, VCHen_HK
dc.contributor.authorTam, PKHen_HK
dc.date.accessioned2010-09-25T16:32:11Z-
dc.date.available2010-09-25T16:32:11Z-
dc.date.issued2003en_HK
dc.identifier.citationThe 2003 International Conference on Enteric Nervous System, Banff, AB., Canada 9-13 July 2003. In Neurogastroenterology and Motility, 2003, v. 15 n. 2, p. 200, abstract no. 16en_HK
dc.identifier.issn1350-1925en_HK
dc.identifier.urihttp://hdl.handle.net/10722/96385-
dc.descriptionpp. 195–237 of this journal issue entitled: Abstracts presented at ENTERIC NERVOUS SYSTEM 2003 An international conference devoted to studies of the enteric nervous system ... 2003-
dc.description.abstractThe neural and glial cells of the intrinsic ganglia of the enteric nervous system (ENS) are derived from the hindbrain neural crest at the vagal level (VNC), but the sacral neural crest (SNC) also has some contribution. The coordination of neural crest migration and the molecular control of their differentiation into specific cell types are not clearly known. Several genes have been found to be involved in ENS development, including Sox10 which when mutated caused megacolon in mice as observed in the Dom mutant. We have identified a VNC specific enhancer element from the mouse Hoxb3 gene, b3-IIIa, which could direct lacZ reporter gene expression in the ENS of transgenic mice. When crossed with the Dom mutant, the hybrid mutant displayed an absence of lacZ marked cells in the hindgut, further con- firming the specificity of this enhancer in the ENS. In order to understand the role of Sox10 during the development of vagal neural crest to the ENS, we have taken a transgenic approach making use of the VNC specific enhancer. We have generated a gain-of-function mutant in which mutant Sox10 with a Dom mutation was ectopically expressed in the vagal neural crest of transgenic mice. The mutants did not have a megacolon phenotype, but immunohistochemical analysis of 14.5 and 16.5 dpc transgenic mutant embryos using anti-neurofilament antibody showed that the ENS development was affected. The distal colons of the mutants were hypoganglionic, with deficient number and complexity of ganglionic plexuses. It is possible that in the transgenic mice, the mutant Sox10 proteins expressed in the VNC may compete with wildtype proteins in a dominant negative manner and as a consequence affect the proliferation and/or differentiation of the enteric ganglia.-
dc.languageengen_HK
dc.publisherBlackwell Publishing Ltd. The Journal's web site is located at http://www.blackwellpublishing.com/journals/NMOen_HK
dc.relation.ispartofNeurogastroenterology and Motilityen_HK
dc.rightsNeurogastroenterology and Motility. Copyright © Blackwell Publishing Ltd.en_HK
dc.titleOver-expression of mutant SOX10 in the vagal neural crest causes hypoganglionic colon development in transgenic miceen_HK
dc.typeConference_Paperen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1350-1925&volume=15&issue=2&spage=200&epage=&date=2003&atitle=Over-expression+of+mutant+SOX10+in+the+vagal+neural+crest+causes+hypoganglionic+colon+development+in+transgenic+miceen_HK
dc.identifier.emailSham, MH: mhsham@hkucc.hku.hken_HK
dc.identifier.emailChan, KK: ken_kkchan@yahoo.comen_HK
dc.identifier.emailChen, AYS: ayschen@hkucc.hku.hken_HK
dc.identifier.emailLui, VCH: vchlui@hkucc.hku.hken_HK
dc.identifier.emailTam, PKH: paultam@hkucc.hku.hken_HK
dc.identifier.authoritySham, MH=rp00380en_HK
dc.identifier.authorityLui, VCH=rp00363en_HK
dc.identifier.authorityTam, PKH=rp00060en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1046/j.1365-2982.2003.00413.x-
dc.identifier.hkuros84289en_HK
dc.identifier.volume15en_HK
dc.identifier.issue2en_HK
dc.identifier.spage200, abstract no. 16en_HK
dc.identifier.epage200, abstract no. 16-

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