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The Role of the Transcriptional Response to DNA Replication Stress

Anna E Herlihy1, Robertus A M de Bruin2,3

  • 1Medical Research Council Laboratory for Molecular Cell Biology, University College London, London WC1E 6BT, UK. a.herlihy.12@ucl.ac.uk.

Genes
|March 4, 2017
PubMed

Insights

DNA replication stress can cause DNA damage. The DNA replication stress checkpoint and its transcriptional response prevent genomic instability by mitigating this damage.

Area of Science:

  • Molecular Biology
  • Genetics
  • Cell Biology

Background:

  • DNA replication stress arises from various factors during DNA replication.
  • The DNA replication stress checkpoint is crucial for preventing DNA damage and genome instability.
  • Post-translational modifications, like phosphorylation, are known regulators of this checkpoint.

Purpose of the Study:

  • To review the cellular response to DNA replication stress.
  • To highlight the specific role of the transcriptional response in the DNA replication stress checkpoint.
  • To explain how this transcriptional response prevents replication stress-induced DNA damage.

Main Methods:

  • This is a review article, synthesizing existing research.
  • Focuses on analyzing current knowledge regarding DNA replication stress response pathways.
  • Examines the interplay between transcription and the replication stress checkpoint.

Main Results:

  • While post-translational modifications are established regulators, transcription plays a newly recognized significant role.
  • The transcriptional response is a key component of the cellular defense against replication stress.
  • This response actively contributes to preventing DNA damage accumulation.

Conclusions:

  • Transcription is integral to the cellular response to DNA replication stress.
  • The DNA replication stress checkpoint's transcriptional activity is vital for maintaining genome stability.
  • Understanding this transcriptional role offers insights into preventing DNA damage.
Keywords:
Chk1DNA replicationDNA replication stressE2F-dependent transcriptionE2F6checkpoint responseoncogene-induced replication stress

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