File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Conference Paper: Analysis of multiple cardiac abnormalities of a mouse mutant Hoxb3lacZ

TitleAnalysis of multiple cardiac abnormalities of a mouse mutant Hoxb3lacZ
Authors
Issue Date2005
PublisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/modo
Citation
The 15th International Society of Developmental Biologist Congress 2005, Sydney, Australia, 3-7 September 2005. In Mechanisms of Development, 2005, v. 122 n. Suppl. 1, p. S62, abstract no. 02-P069 How to Cite?
AbstractWe examined the functional roles of Hoxb3 by generating a Hoxb3lacZ mutant with in-frame insertion of lacZ and neo reporter cassette after the start codon of Hoxb3. In this mutant the coding exons of Hoxb3 have been interrupted by the reporter cassette. Heterozygous Hoxb3lacZ appeared normal, whereas homozygous Hoxb3lacZ/lacZ could not survive till term. There was apparent systemic edema and poor systemic circulation observed in the homozygous mutants at around 15.5 dpc. Whole mount preparation at 9.5 dpc showed a subtle heart tube looping defect in homozygous mutant. Histological analysis of 14.5 dpc Hoxb3lacZ/lacZ showed a range of cardiac abnormalities, including ventricular septal defect (VSD), thinning of the myocardium compact layer and swollen inlet valves. Immunohistochemisty using antibodies against a-smooth muscle actin (a-SMA), a-sarcomeric actin, desmin and Troponin I showed no changes in Hoxb3lacZ/lacZ. Similarity in the expression pattern of both types of actins suggested that the contractility of the mutant heart was not affected. Hoxb3lacZ/lacZ showed remarkedly similar mutant phenotype to TGF-b2 knockout mice. However, analysis of the TGF-b2 expression pattern in homozygous mutants did not show significant difference to the wild type controls, suggesting that other signaling pathways might be involved. As cardiac neural crest contributes to the formation of the outflow tract septation, the abnormal phenotypes observed in the mutant suggest that Hoxb3 may affect cardiac neural crest cells which contribute to cardiac defects of the mutant embryos.
Persistent Identifierhttp://hdl.handle.net/10722/96740
ISBN
ISSN
2015 Impact Factor: 2.041
2015 SCImago Journal Rankings: 1.368

 

DC FieldValueLanguage
dc.contributor.authorSae-Pang, JJen_HK
dc.contributor.authorZhang, Jen_HK
dc.contributor.authorChan, KTen_HK
dc.contributor.authorTsang, WHen_HK
dc.contributor.authorTsang, SLen_HK
dc.contributor.authorSham, MHen_HK
dc.date.accessioned2010-09-25T16:43:12Z-
dc.date.available2010-09-25T16:43:12Z-
dc.date.issued2005en_HK
dc.identifier.citationThe 15th International Society of Developmental Biologist Congress 2005, Sydney, Australia, 3-7 September 2005. In Mechanisms of Development, 2005, v. 122 n. Suppl. 1, p. S62, abstract no. 02-P069-
dc.identifier.isbn1 877040 35 5-
dc.identifier.issn0925-4773-
dc.identifier.urihttp://hdl.handle.net/10722/96740-
dc.description.abstractWe examined the functional roles of Hoxb3 by generating a Hoxb3lacZ mutant with in-frame insertion of lacZ and neo reporter cassette after the start codon of Hoxb3. In this mutant the coding exons of Hoxb3 have been interrupted by the reporter cassette. Heterozygous Hoxb3lacZ appeared normal, whereas homozygous Hoxb3lacZ/lacZ could not survive till term. There was apparent systemic edema and poor systemic circulation observed in the homozygous mutants at around 15.5 dpc. Whole mount preparation at 9.5 dpc showed a subtle heart tube looping defect in homozygous mutant. Histological analysis of 14.5 dpc Hoxb3lacZ/lacZ showed a range of cardiac abnormalities, including ventricular septal defect (VSD), thinning of the myocardium compact layer and swollen inlet valves. Immunohistochemisty using antibodies against a-smooth muscle actin (a-SMA), a-sarcomeric actin, desmin and Troponin I showed no changes in Hoxb3lacZ/lacZ. Similarity in the expression pattern of both types of actins suggested that the contractility of the mutant heart was not affected. Hoxb3lacZ/lacZ showed remarkedly similar mutant phenotype to TGF-b2 knockout mice. However, analysis of the TGF-b2 expression pattern in homozygous mutants did not show significant difference to the wild type controls, suggesting that other signaling pathways might be involved. As cardiac neural crest contributes to the formation of the outflow tract septation, the abnormal phenotypes observed in the mutant suggest that Hoxb3 may affect cardiac neural crest cells which contribute to cardiac defects of the mutant embryos.-
dc.languageengen_HK
dc.publisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/modo-
dc.relation.ispartofMechanisms of Developmenten_HK
dc.titleAnalysis of multiple cardiac abnormalities of a mouse mutant Hoxb3lacZen_HK
dc.typeConference_Paperen_HK
dc.identifier.emailZhang, J: herbertjzhang@hotmail.comen_HK
dc.identifier.emailChan, KT: ktchan@hkucc.hku.hken_HK
dc.identifier.emailTsang, SL: sltsang@HKUSUA.hku.hken_HK
dc.identifier.emailSham, MH: mhsham@hkucc.hku.hken_HK
dc.identifier.authoritySham, MH=rp00380en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.mod.2005.06.010-
dc.identifier.hkuros111947en_HK

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats