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Ciliopathy Protein Tmem107 Plays Multiple Roles in Craniofacial Development.

P Cela1,2, M Hampl1,3, N A Shylo4

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|September 28, 2017
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Summary
This summary is machine-generated.

Transmembrane protein 107 (TMEM107) is crucial for craniofacial development. Its absence in mice causes severe defects, including cleft palate, by disrupting primary cilia function and signaling pathways essential for embryonic development.

Keywords:
cell signalingcraniofacial anomaliesgrowth/developmentmineralized tissue/developmentoral pathologyorofacial clefts

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Area of Science:

  • Developmental Biology
  • Cell Biology
  • Genetics

Background:

  • Ciliopathies are a group of human diseases stemming from defects in primary cilia, essential organelles for sensing cellular environments.
  • Transmembrane protein 107 (TMEM107) localizes to primary cilia and is implicated in ciliopathies like oral-facial-digital syndrome.

Purpose of the Study:

  • To investigate the role of Tmem107 in craniofacial development, specifically palate formation, using a Tmem107 knockout mouse model.
  • To elucidate the underlying mechanisms of craniofacial abnormalities caused by Tmem107 deficiency.

Main Methods:

  • Generation and analysis of Tmem107 knockout (Tmem107-/-) mouse embryos.
  • Detailed morphological and skeletal analysis of craniofacial structures.
  • Investigation of gene expression patterns (SOX2, SOX9, Shh, Gli1) and primary cilia morphology.

Main Results:

  • Tmem107-/- mice exhibited severe craniofacial defects, including cleft lip, exencephaly, and microphthalmia.
  • Palate development was impaired, leading to cleft secondary palate due to abnormal mesenchymal proliferation and horizontalization.
  • Region-specific alterations in primary cilia morphology and disrupted expression of key developmental genes (SOX2, SOX9, Shh, Gli1) were observed.

Conclusions:

  • TMEM107 is essential for normal craniofacial development, particularly palate formation.
  • Tmem107 deficiency leads to region-specific primary cilia defects, impacting signaling pathways and causing complex developmental abnormalities.
  • These findings highlight TMEM107's critical role in embryonic development and provide insights into ciliopathy pathogenesis.