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Creators/Authors contains: "Liang, Tian"

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  1. Free, publicly-accessible full text available March 8, 2024
  2. Abstract

    Mutations of Odontogenesis-Associated Phosphoprotein (ODAPH, OMIM *614829) cause autosomal recessive amelogenesis imperfecta, however, the function of ODAPH during amelogenesis is unknown. Here we characterized normalOdaphexpression by in situ hybridization, generatedOdaphtruncation mice using CRISPR/Cas9 to replace the TGC codon encoding Cys41 into a TGA translation termination codon, and characterized and compared molar and incisor tooth formation inOdaph+/+,Odaph+/C41*, andOdaphC41*/C41*mice. We also searched genomes to determine when Odaph first appeared phylogenetically. We determined that tooth development inOdaph+/+andOdaph+/C41*mice was indistinguishable in all respects, so the condition in mice is inherited in a recessive pattern, as it is in humans.Odaphis specifically expressed by ameloblasts starting with the onset of post-secretory transition and continues until mid-maturation. Based upon histological and ultrastructural analyses, we determined that the secretory stage of amelogenesis is not affected inOdaphC41*/C41*mice. The enamel layer achieves a normal shape and contour, normal thickness, and normal rod decussation. The fundamental problem inOdaphC41*/C41*mice starts during post-secretory transition, which fails to generate maturation stage ameloblasts. At the onset of what should be enamel maturation, a cyst forms that separates flattened ameloblasts from the enamel surface. The maturation stage fails completely.

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