• Login
    View Item 
    •   Home
    • Centers & Institutes
    • Institute of Molecular Medicine and Genetics
    • Institute of Molecular Medicine and Genetics: Faculty Research and Presentations
    • View Item
    •   Home
    • Centers & Institutes
    • Institute of Molecular Medicine and Genetics
    • Institute of Molecular Medicine and Genetics: Faculty Research and Presentations
    • View Item
    JavaScript is disabled for your browser. Some features of this site may not work without it.

    Browse

    All of Scholarly CommonsCommunitiesTitleAuthorsIssue DateSubmit DateSubjectsThis CollectionTitleAuthorsIssue DateSubmit DateSubjects

    My Account

    LoginRegister

    About

    AboutCreative CommonsAugusta University LibrariesUSG Copyright Policy

    Statistics

    Display statistics

    Gap Junctionâ mediated Cellâ Cell Communication Modulates Mouse Neural Crest Migration

    • CSV
    • RefMan
    • EndNote
    • BibTex
    • RefWorks
    Thumbnail
    Name:
    9809035.pdf
    Size:
    669.5Kb
    Format:
    PDF
    Download
    Authors
    Huang, G.Y.
    Cooper, E.S.
    Waldo, K.
    Kirby, M.L.
    Gilula, N.B.
    Lo, C.W.
    Issue Date
    1998-12-14
    URI
    http://hdl.handle.net/10675.2/545
    
    Metadata
    Show full item record
    Abstract
    Previous studies showed that conotruncal heart malformations can arise with the increase or decrease in a1 connexin function in neural crest cells. To elucidate the possible basis for the quantitative requirement for a1 connexin gap junctions in cardiac development, a neural crest outgrowth culture system was used to examine migration of neural crest cells derived from CMV43 transgenic embryos overexpressing a1 connexins, and from a1 connexin knockout (KO) mice and FC transgenic mice expressing a dominant-negative a1 connexin fusion protein. These studies showed that the migration rate of cardiac neural crest was increased in the CMV43 embryos, but decreased in the FC transgenic and a1 connexin KO embryos. Migration changes occurred in step with connexin gene or transgene dosage in the homozygous vs. hemizygous a1 connexin KO and CMV43 embryos, respectively. Dye coupling analysis in neural crest cells in the outgrowth cultures and also in the living embryos showed an elevation of gap junction communication in the CMV43 transgenic mice, while a reduction was observed in the FC transgenic and a1 connexin KO mice. Further analysis using oleamide to downregulate gap junction communication in nontransgenic outgrowth cultures showed that this independent method of reducing gap junction communication in cardiac crest cells also resulted in a reduction in the rate of crest migration. To determine the possible relevance of these findings to neural crest migration in vivo, a lacZ transgene was used to visualize the distribution of cardiac neural crest cells in the outflow tract. These studies showed more lacZ-positive cells in the outflow septum in the CMV43 transgenic mice, while a reduction was observed in the a1 connexin KO mice. Surprisingly, this was accompanied by cell proliferation changes, not in the cardiac neural crest cells, but in the myocardium - an elevation in the CMV43 mice vs. a reduction in the a1 connexin KO mice. The latter observation suggests that cardiac neural crest cells may have a role in modulating growth and development of non-neural crest- derived tissues. Overall, these findings suggest that gap junction communication mediated by a1 connexins plays an important role in cardiac neural crest migration. Furthermore, they indicate that cardiac neural crest perturbation is the likely underlying cause for heart defects in mice with the gain or loss of a1 connexin function.
    Citation
    J Cell Biol. 1998 Dec 14; 143(6):1725-1734
    Collections
    Institute of Molecular Medicine and Genetics: Faculty Research and Presentations

    entitlement

    Related articles

    • Heart malformations in transgenic mice exhibiting dominant negative inhibition of gap junctional communication in neural crest cells.
    • Authors: Sullivan R, Huang GY, Meyer RA, Wessels A, Linask KK, Lo CW
    • Issue date: 1998 Dec 1
    • Alteration in connexin 43 gap junction gene dosage impairs conotruncal heart development.
    • Authors: Huang GY, Wessels A, Smith BR, Linask KK, Ewart JL, Lo CW
    • Issue date: 1998 Jun 1
    • Heart and neural tube defects in transgenic mice overexpressing the Cx43 gap junction gene.
    • Authors: Ewart JL, Cohen MF, Meyer RA, Huang GY, Wessels A, Gourdie RG, Chin AJ, Park SM, Lazatin BO, Villabon S, Lo CW
    • Issue date: 1997 Apr
    • Connexin 43-mediated modulation of polarized cell movement and the directional migration of cardiac neural crest cells.
    • Authors: Xu X, Francis R, Wei CJ, Linask KL, Lo CW
    • Issue date: 2006 Sep
    • Cx43 gap junction gene expression and gap junctional communication in mouse neural crest cells.
    • Authors: Lo CW, Cohen MF, Huang GY, Lazatin BO, Patel N, Sullivan R, Pauken C, Park SM
    • Issue date: 1997
    DSpace software (copyright © 2002 - 2023)  DuraSpace
    Quick Guide | Contact Us
    Open Repository is a service operated by 
    Atmire NV
     

    Export search results

    The export option will allow you to export the current search results of the entered query to a file. Different formats are available for download. To export the items, click on the button corresponding with the preferred download format.

    By default, clicking on the export buttons will result in a download of the allowed maximum amount of items.

    To select a subset of the search results, click "Selective Export" button and make a selection of the items you want to export. The amount of items that can be exported at once is similarly restricted as the full export.

    After making a selection, click one of the export format buttons. The amount of items that will be exported is indicated in the bubble next to export format.