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The biological clock is involved in many aspects of regulating complex physiology in all animals. It was in 1935 when German zoologists, Hans Kalmus and Erwin Bünning, discovered the existence of circadian rhythm in Drosophila melanogaster. However, the internal molecular mechanisms behind the circadian clock remained a mystery until 1984, when Jeffrey C. Hall, Michael Rosbash, and Michael W. Young discovered the expression of the Per gene oscillating over a 24-hour cycle. In subsequent...
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In Vitro Bioluminescence Assay to Characterize Circadian Rhythm in Mammary Epithelial Cells
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Calcium Sets the Clock in Ameloblasts.

Raed Said1,2, Liubov Lobanova2, Silvana Papagerakis3

  • 1Department of Anatomy, Physiology and Pharmacology, College of Medicine, University of Saskatchewan, Saskatoon, SK, Canada.

Frontiers in Physiology
|August 28, 2020
PubMed
Summary
This summary is machine-generated.

Stromal interaction molecule 1 (STIM1) disruption impairs enamel formation by affecting the ameloblast circadian clock. This study reveals STIM1-mediated amelogenesis imperfecta is linked to dysregulated circadian genes and signaling pathways.

Keywords:
STIM1ameloblastamelogenesisamelogenesis imperfectacalciumcircadian clockenamelstore operated Ca2+ channels

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Area of Science:

  • Cell Biology
  • Genetics
  • Developmental Biology

Background:

  • Stromal interaction molecule 1 (STIM1) is crucial for store-operated calcium entry (SOCE).
  • Mutations in STIM1 cause severe enamel hypomineralization (amelogenesis imperfecta), but underlying mechanisms are unclear.
  • Circadian clock signaling influences enamel mineralization, yet its connection to STIM1-mediated amelogenesis imperfecta is unknown.

Purpose of the Study:

  • To investigate the relationship between SOCE and the circadian clock during tooth enamel formation.
  • To elucidate the molecular mechanisms linking STIM1 dysfunction to amelogenesis imperfecta.

Main Methods:

  • Generated ameloblast-specific Stim1 knockout mice (Stim1 cKO).
  • Analyzed circadian gene expression using RNA microarray of 84 genes in Stim1 cKO ameloblasts.
  • Validated gene expression changes via qRT-PCR and immunohistochemistry.

Main Results:

  • Stim1 deletion upregulated the core circadian activator Bmal1 and downregulated the inhibitor Per2.
  • SOCE disruption led to dysregulation of circadian regulators MAPK14 and TGF-β1.
  • MAPK14 and TGF-β1 pathways are implicated in enamel secretion and amelogenesis imperfecta.

Conclusions:

  • Disruption of SOCE significantly impacts the ameloblast molecular circadian clock.
  • Alterations in the circadian clock may contribute to the development of STIM1-mediated amelogenesis imperfecta.