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Push back to respond better: regulatory inhibition of the DNA double-strand break response

Stephanie Panier1, Daniel Durocher

  • 11] The Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, 600 University Avenue, Toronto, Ontario M5G 1X5, Canada. [2] Present address: DNA Damage Response Laboratory, London Research Institute, Cancer Research UK, Clare Hall, South Mimms, London EN6 3LD, UK.

Nature Reviews. Molecular Cell Biology
|September 5, 2013
PubMed

Insights

DNA double-strand breaks (DSBs) trigger cell death and cancer. Pathways controlling DNA damage response must be sensitive, selective, and reversible, using post-translational modifications to maintain genome integrity.

Area of Science:

  • Molecular Biology
  • Genetics
  • Cell Biology

Background:

  • DNA double-strand breaks (DSBs) are critical DNA lesions.
  • Unrepaired DSBs can lead to cell death or oncogenic genome rearrangements.
  • Effective DNA damage response pathways are essential for maintaining genome integrity.

Purpose of the Study:

  • To explore the regulatory mechanisms of DNA damage response pathways.
  • To understand how sensitivity, selectivity, and reversibility are achieved in DNA repair.
  • To highlight the role of post-translational modifications in controlling DNA damage signaling.

Main Methods:

  • Review of current literature on DNA damage response pathways.
  • Analysis of signaling networks involving phosphorylation, ubiquitylation, and acetylation.
  • Examination of regulatory checkpoints in DNA repair.

Main Results:

  • DNA damage response pathways require precise control to prevent deleterious effects.
  • Positive and negative regulatory mechanisms, including post-translational modifications, are crucial.
  • Establishing boundaries for the response is key to limiting damage signaling.

Conclusions:

  • A balance of sensitivity and selectivity is achieved through complex regulatory networks.
  • Post-translational modifications are central to the dynamic control of DNA repair.
  • Effective management of DNA lesions is vital for preventing genomic instability and cancer.

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