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Sustained E2F-Dependent Transcription Is a Key Mechanism to Prevent Replication-Stress-Induced DNA Damage

Cosetta Bertoli1, Anna E Herlihy1, Betheney R Pennycook1

  • 1MRC Laboratory for Molecular Cell Biology , University College London, London WC1E 6BT, UK.

Cell Reports
|May 11, 2016
PubMed

Insights

Transcriptional control, particularly E2F-dependent transcription, is vital for managing DNA replication stress and preventing cancer. Cells with oncogene-induced stress rely on E2F activity to limit DNA damage.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Genomics

Background:

  • DNA replication stress is a known driver of genomic instability and cancer initiation.
  • Post-translational modifications are critical for cellular responses to replication stress.
  • The role of transcriptional control in replication stress response is less understood.

Purpose of the Study:

  • To investigate the role of transcriptional control in replication stress outcomes.
  • To determine the necessity and sufficiency of E2F-dependent transcription in cellular checkpoints.
  • To elucidate the function of E2F activity in oncogene-induced replication stress.

Main Methods:

  • Analysis of E2F-dependent transcription during replication stress.
  • Assessment of checkpoint functions including fork stalling, stabilization, and resolution.
  • Investigation of DNA damage levels in the context of oncogene-induced stress.

Main Results:

  • Transcriptional control plays a more significant role in replication stress than previously thought.
  • Sustained E2F-dependent transcription is essential and sufficient for key checkpoint functions.
  • E2F activity is required to limit DNA damage in oncogene-induced replication stress.

Conclusions:

  • Cells experiencing oncogene-induced replication stress become dependent on E2F activity for survival.
  • E2F-dependent transcription is a critical regulator of the cellular response to replication stress.
  • This highlights a novel mechanism linking transcriptional regulation to cancer development.

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