Generation and characterization of a novel neural crest marker allele, Inka1-LacZ, reveals a role for Inka1 in mouse neural tube closure

Authors

  • Bethany S. Reid,

    1. Department of Craniofacial Biology and Cell and Developmental Biology, University of Colorado Denver, Aurora, Colorado
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  • Thomas D. Sargent,

    1. Laboratory of Molecular Genetics, NICHD, NIH, Bethesda, Maryland
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  • Trevor Williams

    Corresponding author
    1. Department of Craniofacial Biology and Cell and Developmental Biology, University of Colorado Denver, Aurora, Colorado
    • Department of Craniofacial Biology and Cell and Developmental Biology, University of Colorado Denver, Mailstop 8120, 12801 East 17th Avenue, P.O. Box 6511, Aurora, CO 80045
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Abstract

Previous studies identified Inka1 as a gene regulated by AP-2α in the neural crest required for craniofacial morphogenesis in fish and frog. Here, we extend the analysis of Inka1 function and regulation to the mouse by generating a LacZ knock-in allele. Inka1-LacZ allele expression occurs in the cephalic mesenchyme, heart, and paraxial mesoderm prior to E8.5. Subsequently, expression is observed in the migratory neural crest cells and their derivatives. Consistent with expression of Inka1 in tissues of the developing head during neurulation, a low percentage of Inka1−/− mice show exencephaly while the remainder are viable and fertile. Further studies indicate that AP-2α is not required for Inka1 expression in the mouse, and suggest that there is no significant genetic interaction between these two factors during embryogenesis. Together, these data demonstrate that while the expression domain of Inka1 is conserved among vertebrates, its function and regulation are not. Developmental Dynamics 239:1188–1196, 2010. © 2010 Wiley-Liss, Inc.

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