<i>Gbx2</i>is required for the morphogenesis of the mouse inner ear: a downstream candidate of hindbrain signaling

DOI PDF 被引用文献4件
  • Zhengshi Lin
    Laboratory of Molecular Biology, National Institutes on Deafness and Other Communication Disorders, National Institutes of Health, Bethesda, MD 20850, USA
  • Raquel Cantos
    Laboratory of Molecular Biology, National Institutes on Deafness and Other Communication Disorders, National Institutes of Health, Bethesda, MD 20850, USA
  • Maria Patente
    Laboratory of Molecular Biology, National Institutes on Deafness and Other Communication Disorders, National Institutes of Health, Bethesda, MD 20850, USA
  • Doris K. Wu
    Laboratory of Molecular Biology, National Institutes on Deafness and Other Communication Disorders, National Institutes of Health, Bethesda, MD 20850, USA

抄録

<jats:p>Gbx2 is a homeobox-containing transcription factor that is related to unplugged in Drosophila. In mice, Gbx2 and Otx2 negatively regulate each other to establish the mid-hindbrain boundary in the neural tube. Here, we show that Gbx2 is required for the development of the mouse inner ear. Absence of the endolymphatic duct and swelling of the membranous labyrinth are common features in Gbx2-/- inner ears. More severe mutant phenotypes include absence of the anterior and posterior semicircular canals, and a malformed saccule and cochlear duct. However, formation of the lateral semicircular canal and its ampulla is usually unaffected. These inner ear phenotypes are remarkably similar to those reported in kreisler mice, which have inner ear defects attributed to defects in the hindbrain. Based on gene expression analyses, we propose that activation of Gbx2 expression within the inner ear is an important pathway whereby signals from the hindbrain regulate inner ear development. In addition, our results suggest that Gbx2 normally promotes dorsal fates such as the endolymphatic duct and semicircular canals by positively regulating genes such as Wnt2b and Dlx5. However, Gbx2 promotes ventral fates such as the saccule and cochlear duct, possibly by restricting Otx2 expression.</jats:p>

収録刊行物

  • Development

    Development 132 (10), 2309-2318, 2005-05-15

    The Company of Biologists

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