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Slc26a3/Dra and Slc26a6 in Murine Ameloblasts.

R Jalali1, B Zandieh-Doulabi1, P K DenBesten2

  • 1Department of Oral Cell Biology, Academic Centre for Dentistry Amsterdam, University of Amsterdam, and MOVE Research Institute, VU University Amsterdam, Amsterdam, Netherlands.

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|September 24, 2015
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Summary

Maturation ameloblasts use multiple Slc26a anion exchangers, including Dra and Slc26a6, to secrete bicarbonate for dental enamel formation. While individually not critical, these proteins can functionally compensate for each other, ensuring proper enamel mineralization.

Keywords:
Dra-null miceSlc26a6-null miceenamel organimmunolocalizationmicro–computed tomographymineralization

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Area of Science:

  • Biochemistry
  • Cell Biology
  • Developmental Biology

Background:

  • Enamel mineralization requires proton buffering by maturation ameloblasts.
  • Existing evidence suggests bicarbonate secretion into enamel, but the mechanism remains unclear.
  • Solute carrier (Slc) family 26A anion exchangers (Dra, Slc26a6, pendrin) mediate Cl(-)/HCO3 (-) exchange.

Purpose of the Study:

  • To test the hypothesis that maturation ameloblasts express Dra and Slc26a6 for bicarbonate secretion.
  • To investigate the roles of Dra and Slc26a6 in dental enamel formation.
  • To explore functional compensation among Slc26a isoforms in ameloblasts.

Main Methods:

  • Real-time polymerase chain reaction (PCR) to detect mRNA transcripts for Dra and Slc26a6.
  • Western blotting to confirm protein expression of Dra and Slc26a6.
  • Immunolocalization of Dra and Slc26a6 in ameloblasts.
  • Analysis of null mutation mice (Dra, Slc26a6, Ae2a,b, Cftr) using micro-computed tomography (micro-CT) and protein level assessments.

Main Results:

  • Dra and Slc26a6 mRNA and protein were detected in mouse incisor enamel organs, localized to maturation stage ameloblasts.
  • Mice lacking either Dra or Slc26a6 exhibited normal dental and skeletal phenotypes with no changes in mineral density.
  • In Slc26a6-null mice, Dra and pendrin protein levels increased, while Slc26a6 protein was reduced in Dra-null mice, indicating compensatory expression.

Conclusions:

  • Ameloblasts express Dra, pendrin, or Slc26a6, but none are individually essential for enamel formation.
  • Slc26a isoforms (Dra, pendrin, Slc26a6) demonstrate functional compensation in ameloblasts.
  • These findings elucidate potential mechanisms for bicarbonate transport critical for dental enamel development.