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The two edges of the ATM sword: co-operation between repair and checkpoint functions

Markus Löbrich1, Penny A Jeggo

  • 1Fachrichtung Biophysik, Universität des Saarlandes, Homburg/Saar, Germany. p.a.jeggo@sussex.ac.uk

Radiotherapy and Oncology : Journal of the European Society for Therapeutic Radiology and Oncology
|July 20, 2005
PubMed

Insights

Ataxia-telangiectasia mutated (ATM) protein coordinates DNA repair and cell cycle arrest following DNA double-strand breaks (DSBs). This dual function enhances cell survival and cancer avoidance after irradiation.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Genetics

Background:

  • ATM is a key protein in the DNA damage response pathway.
  • It regulates cell cycle checkpoints and apoptosis after DNA double-strand breaks (DSBs).
  • ATM also plays a role in processing difficult-to-ligate DNA ends.

Purpose of the Study:

  • To explore the novel function of ATM in DNA end processing.
  • To discuss ATM's contribution to cell survival after ionizing irradiation.
  • To highlight ATM's role in cancer avoidance.

Main Methods:

  • Review of recent studies on ATM function.
  • Analysis of ATM's role in DNA repair mechanisms.
  • Discussion of ATM's checkpoint and repair coordination.

Main Results:

  • ATM facilitates the repair of a subset of DSBs that are otherwise difficult to ligate.
  • The nuclease Artemis is involved in this ATM-regulated processing.
  • In the absence of ATM's processing function, DSBs may remain unrejoined or be misrejoined.

Conclusions:

  • ATM's checkpoint function is crucial for its DNA repair capabilities.
  • The coordinated action of ATM's repair and checkpoint functions enhances survival after irradiation.
  • This integrated function of ATM is vital for cancer avoidance.

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