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Polo-like kinase-1 is a target of the DNA damage checkpoint

V A Smits1, R Klompmaker, L Arnaud

  • 1Jordan Laboratory, Department of Hematology, University Medical Centre Utrecht G 03.647, P.O. Box 85500, 3508 GA Utrecht, The Netherlands.

Nature Cell Biology
|September 12, 2000
PubMed

Insights

DNA damage inhibits Polo-like kinase-1 (Plk1) activity during G2 and mitosis, blocking cell cycle progression. Activated Plk1 mutants override DNA damage-induced arrests, highlighting Plk1 as a key target of the DNA damage checkpoint.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Genetics

Background:

  • Polo-like kinases (PLKs) are crucial regulators of mitosis, involved in centrosome maturation, spindle formation, and mitotic exit.
  • The PLK Cdc5 in yeast is known to be regulated by the DNA damage checkpoint.

Purpose of the Study:

  • To investigate the effects of DNA damage on Polo-like kinase-1 (Plk1) in human cell lines.
  • To determine Plk1's role as a target of the DNA damage checkpoint.

Main Methods:

  • Treatment of human cell lines with DNA-damaging agents.
  • Analysis of Plk1 activity and cell cycle progression.
  • Expression of Plk1 mutants with altered T-loop phosphorylation sites.

Main Results:

  • DNA damage inhibits Plk1 activity in both G2 and mitotic phases.
  • DNA damage induces cell cycle arrest at G2 and blocks mitotic exit.
  • Plk1 mutants resistant to DNA damage inhibition can override G2 arrest.

Conclusions:

  • Plk1 is a critical target of the DNA damage checkpoint.
  • Inhibition of Plk1 by DNA damage contributes to cell cycle arrest in G2 and mitosis.
  • Plk1 plays a significant role in coordinating cell cycle progression with DNA damage response.

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