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Regulation of a transcription factor network by Cdk1 coordinates late cell cycle gene expression

Benjamin D Landry1, Claudine E Mapa, Heather E Arsenault

  • 1Program in Gene Function and Expression, University of Massachusetts Medical School, Worcester, MA, USA.

The EMBO Journal
|April 10, 2014
PubMed

Insights

Cyclin-dependent kinase 1 (Cdk1) phosphorylation of transcription factors (TFs) is crucial for regulating gene expression during cell division. This regulation ensures proper mitotic progression and genome stability in yeast.

Area of Science:

  • Molecular and Cellular Biology
  • Yeast Genetics
  • Cell Cycle Regulation

Background:

  • Genome stability relies on precise coordination between chromosome segregation and mitotic events.
  • Cyclin-dependent kinase 1 (Cdk1) regulates the expression of late cell cycle genes through phosphorylation of transcription factors (TFs).
  • The precise impact of Cdk1 phosphorylation on many key TFs remains largely uncharacterized.

Purpose of the Study:

  • To investigate the functional consequences of Cdk1-mediated phosphorylation on S-phase transcription factors.
  • To elucidate the role of Cdk1 in regulating gene expression networks essential for cell division.
  • To understand how Cdk1 phosphorylation impacts the activity and stability of key transcriptional regulators.

Main Methods:

  • Utilized budding yeast (Saccharomyces cerevisiae) as a model organism.
  • Generated mutants deficient in Cdk1-mediated phosphorylation of specific S-phase TFs.
  • Assessed gene expression changes, mitotic progression, and cellular fitness.
  • Analyzed TF degradation, promoter occupancy, and transcriptional activity.

Main Results:

  • Elimination of Cdk1 phosphorylation in four S-phase TFs led to decreased late cell cycle gene expression, delayed mitosis, and reduced yeast fitness.
  • Impaired phosphorylation blocked the degradation of these TFs, altering their regulatory functions.
  • Phosphorylation-deficient repressors (Yox1, Yhp1) showed increased promoter binding and reduced target gene expression.
  • Cdk1 phosphorylation of the activator Hcm1 had dual effects: N-terminal phosphorylation promoted degradation, while C-terminal phosphorylation was essential for activity.

Conclusions:

  • Cdk1 promotes gene expression by activating transcriptional activators and inactivating transcriptional repressors via phosphorylation.
  • Coordinated regulation of the TF network by Cdk1 is essential for accurate cell division and genome stability.
  • Cdk1 acts as a critical switch, modulating TF activity and stability to ensure proper cell cycle progression.

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