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Updated: Feb 4, 2026

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Persistent repair intermediates induce senescence.

F M Feringa1, J A Raaijmakers1, M A Hadders2

  • 1Oncode Institute, Division of Cell Biology, Netherlands Cancer Institute, 1066CX, Amsterdam, The Netherlands.

Nature Communications
|September 27, 2018
PubMed
Summary
This summary is machine-generated.

Cell cycle arrest after DNA damage depends on DNA repair speed. Delayed repair in G2 phase promotes cell cycle exit, indicating cells can assess repair difficulty.

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Area of Science:

  • Cell Biology
  • Molecular Biology
  • Genetics

Background:

  • Double-stranded DNA breaks (DSBs) trigger cell cycle checkpoints, notably in G2 phase, leading to arrest.
  • While arrest can be reversible for recovery, G2 cells may permanently exit the cell cycle via senescence or apoptosis.
  • The decision-making process for cell cycle recovery versus withdrawal remains unclear.

Purpose of the Study:

  • To investigate the factors governing the G2 cell cycle decision following DNA damage.
  • To determine the role of DNA repair progression in cell cycle withdrawal.

Main Methods:

  • Analysis of DNA repair kinetics and associated signaling pathways in G2-arrested cells.
  • Investigating the impact of homologous recombination (HR) repair delays on cell fate.
  • Quantifying DNA resection levels and ATR signaling activation.

Main Results:

  • Cell cycle withdrawal in G2 is critically dependent on the progression of DNA repair.
  • Delayed HR-mediated repair of DSBs leads to increased DNA resection and enhanced ATR signaling.
  • Elevated ATR signaling results in increased p21 levels, driving cell cycle exit.

Conclusions:

  • Cells can discriminate between repairable and difficult-to-repair DNA breaks during the repair process.
  • The rate of DNA repair progression influences the decision between cell cycle recovery and permanent exit.
  • ATR signaling and p21 levels act as key mediators in this decision-making pathway.