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Ift88 limits bone formation in maxillary process through suppressing apoptosis.

Momoko Watanabe1, Maiko Kawasaki2, Katsushige Kawasaki3

  • 1Division of Oral Anatomy, Department of Oral Biological Science, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan; Division of Oral and Maxillofacial Surgery, Department of Health Science, Course for Oral science, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan.

Archives of Oral Biology
|March 18, 2019
PubMed
Summary
This summary is machine-generated.

Mesenchymal deletion of Ift88 in mice leads to excess maxillary bone formation by suppressing apoptosis. This suggests Ift88 is crucial for regulating bone development in the craniofacial region.

Keywords:
ApoptosisBone formationIft88Maxillary processPrimary cilia

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Area of Science:

  • Craniofacial development
  • Bone biology
  • Cell biology

Background:

  • Primary cilia are essential for craniofacial development and bone formation.
  • Defects in primary cilia cause ciliopathies, a spectrum of congenital diseases.
  • The specific role of primary cilia in maxillary bone development remains unclear.

Purpose of the Study:

  • To investigate the role of Ift88, a key component of primary cilia, in maxillary bone development.
  • To determine the molecular mechanisms by which Ift88 influences maxillary bone formation and craniofacial morphogenesis.

Main Methods:

  • Generated mesenchymal conditional knockout mice lacking Ift88 using Wnt1Cre driver (Ift88fl/fl;Wnt1Cre).
  • Analyzed maxillary bone development, apoptosis, and palatal formation in mutant mice.
  • Created compound mutants (Ift88fl/fl;Wnt1Cre;p53-/-) to assess the role of apoptosis in observed phenotypes.

Main Results:

  • Mice with mesenchymal Ift88 deletion exhibited cleft palate and excess bone formation in the maxillary process.
  • Ectopic apoptosis was observed in the developing Ift88 mutant maxillary process.
  • Reducing apoptosis in Ift88 mutant mice (Ift88fl/fl;Wnt1Cre;p53-/-) rescued the excess bone formation but not the cleft palate.

Conclusions:

  • Ift88 is essential for regulating bone formation in the maxillary process.
  • Ift88 limits maxillary bone formation by promoting apoptosis.
  • The observed cleft palate phenotype is independent of Ift88-mediated apoptosis and excess bone formation.