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Restarting Stalled Replication Forks02:37

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DNA replication is initiated at sites containing predefined DNA sequences known as origins of replication. DNA is unwound at these sites by the minichromosome maintenance (MCM) helicase and other factors such as Cdc45 and the associated GINS complex.The unwound single strands are protected by replication protein A (RPA) until DNA polymerase starts synthesizing DNA at the 5’ end of the strand in the same direction as the replication fork. To prevent the replication fork from falling apart,...
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The basic reaction of homologous recombination (HR) involves two chromatids that contain DNA sequences sharing a significant stretch of identity. One of these sequences uses a strand from another as a template to synthesize DNA in an enzyme-catalyzed reaction. The final product is a novel amalgamation of the two substrates. To ensure an accurate recombination of sequences, HR is restricted to the S and G2 phases of the cell cycle. At these stages, the DNA has been replicated already and the...
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In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
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Because the DNA segments are cut and reorganized in a direction-specific manner, site-specific recombination has emerged as an efficient genetic engineering technique. Flippase and Cyclization recombinases or Flp and Cre, respectively, are two members of the tyrosine recombinase family derived from bacteriophages, that are used to mediate site-specific DNA insertions, deletions, and targeted expression of proteins in mammalian cell lines.
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Related Experiment Video

Updated: Jul 30, 2025

Real-time Observation of the DNA Strand Exchange Reaction Mediated by Rad51
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Noncanonical Roles of RAD51.

Mélissa Thomas1, Caroline Dubacq2, Elise Rabut1

  • 1INSERM U1016, UMR 8104 CNRS, Institut Cochin, Université de Paris Cité, 24 rue du Faubourg St. Jacques, F-75014 Paris, France.

Cells
|May 16, 2023
PubMed
Summary

The protein RAD51 is crucial for DNA repair through homologous recombination (HR). However, its paradoxical lack of cancer predisposition suggests diverse, noncanonical functions beyond DNA strand exchange, impacting genome plasticity and development.

Keywords:
Fanconi anemiaRAD51RNA:DNA hybridscancer predispositioncongenital mirror syndromedouble-strand break repairgenome instabilityhomologous recombinationpost-replication repairreplication stress

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Last Updated: Jul 30, 2025

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Area of Science:

  • Molecular Biology
  • Genetics
  • Cell Biology

Background:

  • Homologous recombination (HR) is vital for genome stability.
  • RAD51 protein is central to HR's strand invasion/exchange activity.
  • Mutations in HR genes are linked to cancer, but RAD51 invalidation is not.

Purpose of the Study:

  • To explore the noncanonical roles of RAD51 beyond its canonical function in HR.
  • To address the "RAD51 paradox" concerning its role in cancer predisposition.
  • To highlight RAD51's diverse functions in genome plasticity and cellular processes.

Main Methods:

  • Literature review of studies on RAD51 function.
  • Analysis of RAD51's roles in DNA repair pathways.
  • Examination of RAD51's involvement in replication fork management and RNA-mediated processes.

Main Results:

  • RAD51 has noncanonical roles, including preventing mutagenic repair and managing replication fork reversal.
  • RAD51 participates in RNA-mediated processes.
  • RAD51 pathogenic variants are linked to congenital mirror movement syndrome, indicating a role in brain development.

Conclusions:

  • RAD51 exhibits multiple functions independent of its catalytic strand invasion/exchange activity.
  • These noncanonical roles contribute significantly to genome plasticity.
  • Understanding RAD51's multifaceted nature is crucial for comprehending its impact on health and disease.