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Mouse period 2 mRNA circadian oscillation is modulated by PTB-mediated rhythmic mRNA degradation

Kyung-Chul Woo1, Tae-Don Kim, Kyung-Ha Lee

  • 1Department of Life Science, Division of Molecular and Life Science, Pohang University of Science and Technology, Pohang, South Korea.

Nucleic Acids Research
|November 18, 2008
PubMed

Insights

Polypyrimidine tract-binding protein (PTB) regulates circadian oscillations of period 2 (mper2) mRNA. PTB-mediated mRNA decay fine-tunes mper2 oscillations, impacting cell cycle and tumor suppression.

Area of Science:

  • Molecular Biology
  • Chronobiology
  • Gene Regulation

Background:

  • Circadian rhythms are fundamental biological processes driven by core clock genes exhibiting diurnal mRNA oscillations.
  • Period 2 (mper2) is a critical clock gene involved in negative-feedback loops, cell cycle regulation, and tumor suppression.
  • Post-transcriptional regulation, including mRNA decay, plays a role in controlling circadian gene expression.

Purpose of the Study:

  • To investigate the role of 3'-untranslated region (UTR)-dependent mRNA decay in regulating circadian oscillations of period 2 (mper2) mRNA.
  • To identify specific elements and proteins within the mper2 3'UTR that influence mRNA stability and degradation.
  • To elucidate the mechanism by which polypyrimidine tract-binding protein (PTB) affects mper2 circadian rhythms.

Main Methods:

  • RNA interference (RNAi) to deplete PTB levels.
  • Analysis of mper2 mRNA stability and degradation kinetics.
  • Quantitative analysis of cytoplasmic PTB and mper2 mRNA expression profiles during circadian cycles.

Main Results:

  • The CU-rich region and PTB within the mper2 3'UTR are key determinants of mRNA stability and degradation.
  • Depletion of PTB using RNAi leads to significant stabilization of mper2 mRNA.
  • Cytoplasmic PTB exhibits a reciprocal expression pattern to mper2 mRNA during circadian oscillations.
  • PTB depletion increases the peak amplitude of mper2 circadian oscillations.

Conclusions:

  • Post-transcriptional mRNA decay mediated by PTB is a crucial mechanism for fine-tuning circadian oscillations of mper2 mRNA.
  • PTB acts as a negative regulator, dampening the amplitude of circadian mper2 mRNA oscillations.
  • This regulatory pathway highlights the intricate control of circadian gene expression and its potential links to cell cycle and tumor suppression.

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