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Quantitative PCR-based Assay to Measure Sonic Hedgehog Signaling in Cellular Model of Ciliogenesis
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Progressive tooth pattern changes in Cilk1-deficient mice depending on Hedgehog signaling.

Minjae Kyeong1, Ju-Kyung Jeong2, Dinuka Adasooriya1

  • 1Department of Oral Biology, BK21 FOUR Project, Oral Science Research Center, Yonsei University College of Dentistry, Seoul, South Korea.

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|November 30, 2025
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Summary

Loss of Cilk1 kinase disrupts primary cilia function, leading to supernumerary teeth and molar fusion by altering Hedgehog signaling in mice. This reveals Cilk1

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Area of Science:

  • Developmental Biology
  • Cell Biology
  • Genetics

Background:

  • Primary cilia are sensory organelles crucial for developmental signaling pathways like Hedgehog (Hh).
  • Hh pathway dysregulation is linked to abnormal tooth development, including supernumerary teeth and molar fusion.
  • Cilk1 kinase is vital for ciliary transport, and its loss causes ciliopathies, but its role in tooth development is unknown.

Purpose of the Study:

  • To investigate the function of Cilk1 in mammalian tooth development.
  • To elucidate the role of Cilk1-mediated ciliary transport in Hedgehog signaling during odontogenesis.
  • To understand how Cilk1 deficiency impacts tooth patterning and morphology.

Main Methods:

  • Analysis of Cilk1 expression in developing mouse molars.
  • Generation and phenotypic analysis of Cilk1-deficient mice.
  • Assessment of ciliary dynamics and Hedgehog signaling pathway activity (e.g., Ptch1, Sostdc1 expression).
  • Examination of tooth morphology and patterning in wild-type and mutant mice, including compound mutants.

Main Results:

  • Cilk1 is expressed in developing molar epithelium and mesenchyme.
  • Cilk1 deficiency alters ciliary dynamics (reduced frequency, increased length) and downregulates Hh target genes.
  • Loss of Cilk1 leads to diastemal supernumerary teeth formation.
  • Compounded Hh signaling suppression results in enlarged diastemal supernumerary teeth and molar fusion.

Conclusions:

  • Cilk1 is essential for normal tooth development by regulating ciliary function and Hh signaling.
  • Altered Hh signaling levels, influenced by Cilk1, progressively affect tooth patterning, from supernumerary tooth induction to molar fusion.
  • This study identifies a novel role for Cilk1 in controlling tooth morphology through a gradient-dependent Hh signaling mechanism.