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[Regulation of osmolyte transporter gene expression by tonicity]

M Takenaka1, A Yamauchi, E Imai

  • 1First Department of Medicine, Osaka University School of Medicine.

Insights

Cells protect themselves from hypertonic environments by accumulating osmolytes like myo-inositol and betaine using specific transporters. This study identified a tonicity-responsive enhancer (TONE) in the betaine transporter gene (BGT1) that regulates its expression in the kidney.

Area of Science:

  • Cell biology
  • Molecular biology
  • Physiology

Background:

  • Cells accumulate osmolytes (e.g., myo-inositol, betaine, taurine) to counteract hypertonic stress.
  • Osmolyte accumulation is mediated by specific transporters, whose transcription is induced by hypertonicity.
  • Kidney plays a crucial role in osmotic balance and osmolyte transport.

Purpose of the Study:

  • To investigate the transcriptional regulation of osmolyte transporters in response to hypertonicity.
  • To identify and characterize regulatory elements within the betaine transporter (BGT1) gene.
  • To confirm the functional role of identified regulatory elements in vivo.

Main Methods:

  • Expression cloning of osmolyte transporters.
  • In situ hybridization to determine mRNA localization of transporters in the kidney.
  • Gene cloning and 5' flanking region characterization of the BGT1 gene.
  • Analysis of transgenic mice carrying the BGT1 gene's 5' flanking region.

Main Results:

  • Specific transporters for myo-inositol, betaine, and taurine were cloned.
  • Na+/myo-inositol cotransporter and betaine transporter (BGT1) mRNAs were localized to the kidney.
  • A 13 bp tonicity-responsive enhancer (TONE) was identified in the 5' flanking region of the BGT1 gene.
  • Transgenic mice demonstrated inducible reporter expression in the kidney medulla driven by the BGT1 5' flanking region containing TONE.

Conclusions:

  • Hypertonicity induces the transcription of osmolyte transporters.
  • The identified TONE element is a key regulator of BGT1 gene expression in the kidney medulla.
  • This provides a molecular mechanism for kidney adaptation to hypertonic environments.

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