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Cell-cycle-dependent regulation of the human and mouse Tome-1 promoters

Kenichi Yoshida1

  • 1Department of Life Sciences, Faculty of Agriculture, Meiji University, Kawasaki, Kanagawa 214-8571, Japan. yoshida@isc.meiji.ac.jp

FEBS Letters
|March 1, 2005
PubMed

Insights

Trigger of mitotic entry 1 (Tome-1) gene expression is activated during the G2/M phase. Promoter analysis revealed key regulatory elements, including a CCAAT box and a repressor element, crucial for Tome-1

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Genetics

Background:

  • Tome-1 (trigger of mitotic entry 1) regulates cell cycle progression by targeting Wee1 kinase for degradation.
  • Tome-1 itself is degraded by the anaphase-promoting complex (APC) during the G1 phase.
  • Understanding Tome-1 regulation is crucial for comprehending cell cycle control.

Purpose of the Study:

  • To investigate the transcriptional regulation of the Tome-1 gene.
  • To identify key regulatory elements within the human and mouse Tome-1 promoter regions.
  • To elucidate the cell-cycle-dependent control of Tome-1 expression.

Main Methods:

  • Analysis of human and mouse Tome-1 promoter regions.
  • Luciferase reporter assays using synchronized NIH3T3 cells transfected with Tome-1 promoter constructs.
  • Site-directed mutagenesis to assess the function of specific promoter elements.

Main Results:

  • Tome-1 promoter activity is significantly activated during the G2/M phase of the cell cycle.
  • A CCAAT box upstream of the transcription start site is essential for basal promoter activity.
  • A repressor element (cell-cycle-dependent element/cell cycle gene homology region) near the transcription start site controls cell-cycle-dependent regulation.

Conclusions:

  • Tome-1 expression is tightly regulated at the transcriptional level during the cell cycle.
  • Specific promoter elements, including the CCAAT box and a repressor element, are critical for controlling Tome-1's cell-cycle-dependent activity.
  • These findings provide insights into the molecular mechanisms governing mitotic entry.

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