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DNA damage foci in mitosis are devoid of 53BP1

Glyn Nelson1, Matthias Buhmann, Thomas von Zglinicki

  • 1Centre for Integrated Systems Biology of Ageing and Nutrition, Institute for Ageing and Health, Newcastle University, Newcastle upon Tyne, UK.

Cell Cycle (Georgetown, Tex.)
|October 7, 2009
PubMed

Insights

DNA damage response involves 53BP1 protein, crucial for cell cycle arrest. However, 53BP1 recruitment to DNA damage foci is inhibited during G2/M phase, potentially allowing cells to bypass checkpoints.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Genetics

Background:

  • Nuclear DNA damage foci signal ongoing DNA damage response (DDR).
  • DDR is a major inducer of cell cycle arrest, senescence, and apoptosis.
  • 53BP1 is a key mediator in DDR and a component of DNA damage foci.

Purpose of the Study:

  • To investigate the role of 53BP1 recruitment to DNA damage foci during the cell cycle.
  • To determine if cell cycle phase affects 53BP1-mediated DNA damage signaling.

Main Methods:

  • Utilized an AcGFP-53BP1c fluorescent fusion protein to monitor DNA damage.
  • Quantitatively assessed 53BP1 recruitment into gammaH2A.X foci.
  • Analyzed 53BP1 recruitment dynamics across different cell cycle phases, specifically G2/M.

Main Results:

  • Recruitment of 53BP1 into gammaH2A.X-containing DNA damage foci was significantly inhibited during the G2/M phase.
  • This inhibition suggests a potential mechanism for checkpoint bypass.

Conclusions:

  • The cell cycle, particularly G2/M phase, regulates 53BP1 recruitment to DNA damage sites.
  • Inhibition of 53BP1 signaling at G2/M may allow cells with double-strand breaks to proceed through the G2 checkpoint.

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