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Phosphorylation of Plk1 at S137 and T210 is inhibited in response to DNA damage

Lyuben Tsvetkov1, David F Stern

  • 1Department of Pathology, School of Medicine, Yale University, New Haven, Connecticut 06510, USA. lyuben.tsvetkov@yale.edu

Cell Cycle (Georgetown, Tex.)
|December 22, 2004
PubMed

Insights

DNA damage checkpoints regulate Polo-like kinase 1 (Plk1) phosphorylation at serine 137 and threonine 210 during mitosis. Inhibitors of ATM/ATR and Chk1/Chk2 kinases prevent this DNA damage-induced inhibition.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Polo-like kinase 1 (Plk1) is crucial for mitotic progression, regulating entry into mitosis and activating the Cdc2/cyclin B kinase.
  • Plk1 activation occurs via phosphorylation, with threonine 210 identified as a major activation site.
  • DNA damage checkpoints, involving ATM/ATR pathways, inhibit Plk1 activity.

Purpose of the Study:

  • To investigate the in vivo phosphorylation sites of Plk1 during mitosis.
  • To determine how DNA damage affects Plk1 phosphorylation at specific sites.
  • To elucidate the role of DNA damage checkpoints in regulating Plk1 phosphorylation.

Main Methods:

  • In vivo phosphorylation analysis of Plk1.
  • Mutational analysis of Plk1 phosphorylation sites.
  • Treatment with DNA-damaging agents and checkpoint kinase inhibitors (ATM/ATR, Chk1/Chk2).

Main Results:

  • In vivo phosphorylation of Plk1 occurs at serine 137 (S137) and threonine 210 (T210) during mitosis.
  • DNA damage inhibits Plk1 phosphorylation at S137 and T210 in asynchronous cells, but not in mitotic cells.
  • Inhibitors of ATM/ATR and Chk1/Chk2 kinases block the DNA damage-induced inhibition of Plk1 phosphorylation.

Conclusions:

  • DNA damage checkpoints regulate Plk1 phosphorylation at S137 and T210.
  • The regulation of Plk1 phosphorylation by DNA damage checkpoints occurs upstream of Plk1 itself.
  • These findings highlight a mechanism by which DNA damage signaling influences mitotic progression via Plk1.

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