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Restarting Stalled Replication Forks02:37

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Related Experiment Video

Updated: Apr 18, 2026

Direct Restart of a Replication Fork Stalled by a Head-On RNA Polymerase
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Checkpoint-dependent RNR induction promotes fork restart after replicative stress.

Esther C Morafraile1, John F X Diffley2, José Antonio Tercero3

  • 1Instituto de Biología Funcional y Genómica and Departamento de Microbiología y Genética, (CSIC/USAL), Campus Miguel de Unamuno, Salamanca 37007, Spain.

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Summary

Checkpoint kinase Rad53 prevents DNA replication fork degradation and cell death during stress. Rad53 regulates ribonucleotide reductase (RNR) expression, restoring replication fork restart and viability in rad53 mutants.

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Area of Science:

  • Molecular Biology
  • Cell Cycle Regulation
  • DNA Replication Stress Response

Background:

  • Checkpoint kinase Rad53 is essential for managing DNA replication under stress.
  • Rad53 normally prevents Exo1-dependent degradation of replication forks.

Purpose of the Study:

  • To investigate the role of Rad53 in replication restart and cell survival during hydroxyurea (HU) treatment.
  • To elucidate the mechanism by which Rad53 regulates ribonucleotide reductase (RNR) in response to replication stress.

Main Methods:

  • Analysis of rad53 mutants with and without EXO1 deletion.
  • Assessment of cell viability and replication fork restart following HU treatment.
  • Investigation of RNR expression and localization under different genetic conditions.

Main Results:

  • Exo1 deletion prevents fork degradation in rad53 mutants but does not rescue HU sensitivity.
  • Rad53 regulates replication restart via checkpoint-dependent RNR induction.
  • Inducing RNR in exo1 mutants lacking negative regulators rescues rad53 mutant viability and fork restart.

Conclusions:

  • Rad53's role extends beyond preventing fork degradation; it actively promotes replication restart by inducing RNR.
  • Rad53-mediated RNR regulation is critical for cell survival under replicative stress.
  • Targeting RNR expression offers a potential strategy to enhance cell viability during DNA replication stress.