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Use of Trowell-Type Organ Culture to Study Regulation of Dental Stem Cells
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Sox2 contributes to tooth development via Wnt signaling.

Min-Jung Lee1, Eun-Jung Kim1, Keishi Otsu2

  • 1Division in Anatomy and Developmental Biology, Department of Oral Biology, Oral Science Research Center, BK21 PLUS Project, Yonsei University College of Dentistry, 50-1 Yonsei-ro, Seodaemoon-Gu, Seoul, 03722, South Korea.

Cell and Tissue Research
|February 6, 2016
PubMed
Summary

Sox2 is crucial for mouse molar development, regulating cell migration and Wnt signaling. Its absence disrupts these processes, highlighting Sox2

Keywords:
Cell migrationDiI systemSox2ToothWnt signaling

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Area of Science:

  • Developmental Biology
  • Stem Cell Biology
  • Molecular Signaling

Background:

  • Sox2 (Sex-determining region Y-box 2) is a key transcription factor and stem cell marker.
  • It plays a role in epithelial stem cell populations, including those in mouse incisors.
  • Sox2 interacts with β-catenin, modulating Wnt signaling, a critical pathway in development.

Purpose of the Study:

  • To investigate the essential functions of Sox2 in mouse molar development.
  • To elucidate Sox2's role in regulating cell migration during tooth formation.
  • To validate Sox2 as a therapeutic target for modulating Wnt signaling in tooth development.

Main Methods:

  • Temporal knockdown of Sox2 in mouse models.
  • Utilizing a DiI cell tracing system to monitor cell migration patterns.
  • Analyzing the impact of Sox2 on Wnt signaling pathway components, specifically β-catenin.

Main Results:

  • Sox2 is essential for normal mouse molar development.
  • Knockdown of Sox2 significantly impairs cell migration between developing molars (molar 1 to molar 2).
  • Sox2 knockdown leads to the degradation of Wnt signaling, evidenced by impaired β-catenin function.

Conclusions:

  • Sox2 is indispensable for cell migration during mouse tooth development.
  • Disruption of Sox2 function leads to a breakdown in Wnt signaling.
  • These findings underscore Sox2's critical role and potential as a target in Wnt-mediated tooth development.