The function and regulation of TBX22 in avian frontonasal morphogenesis

Authors

  • Norihisa Higashihori,

    1. Department of Oral Health Sciences, Life Sciences Institute, University of British Columbia, Vancouver, Canada
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  • Marcela Buchtová,

    1. Department of Oral Health Sciences, Life Sciences Institute, University of British Columbia, Vancouver, Canada
    Current affiliation:
    1. Institute of Animal Physiology and Genetics, Academy of Sciences of the Czech Republic and Department of Anatomy, Histology and Embryology, University of Veterinary and Pharmaceutical Sciences, Brno, Czech Republic
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  • Joy M. Richman

    Corresponding author
    1. Department of Oral Health Sciences, Life Sciences Institute, University of British Columbia, Vancouver, Canada
    • Department of Oral Health Sciences, Life Sciences Institute, UBC, 2350 Health Sciences Mall, Vancouver, BC V6T 1Z3
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Abstract

The frontonasal mass gives rise to the facial midline and fuses with the maxillary prominence to form the upper lip. Here we focus on the regulation and function of TBX22, a repressor dynamically expressed in the frontonasal mass. Both FGF and Noggin (a BMP antagonist) strongly induce gTBX22, however, each has opposite effects on morphogenesis - Noggin inhibits whereas FGF stimulates growth. To determine whether TBX22 mediates these effects, we used retroviruses to locally increase expression levels. RCAS::hTBX22 decreased proliferation, reduced expression of MSX2 and DLX5 and caused cleft lip. Decreased levels of endogenous gTBX22 were also observed but were not the primary cause of the phenotype as determined in rescue experiments. Our data suggest that genetic or environmental insults such as those affecting the BMP pathway could lead to a gain-of-function of TBX22 and predispose an individual to cleft lip. Developmental Dynamics 239:458–473, 2010. © 2009 Wiley-Liss, Inc.

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