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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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An organism’s genome needs to be duplicated in an efficient and error-free manner for its growth and survival. The replication fork is a Y-shaped active region where two strands of DNA are separated and replicated continuously. The coupling of DNA unzipping and complementary strand synthesis is a characteristic feature of a replication fork.   Organisms with small circular DNA, such as E. coli, often have a single origin of replication; therefore, they have only two replication...
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Updated: Jun 15, 2025

Author Spotlight: Unveiling the Role of SNF2L in Replication Fork Stability and Genome Duplication
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RAD51 protects abasic sites to prevent replication fork breakage.

Yodhara Wijesekara Hanthi1, Miguel Angel Ramirez-Otero1, Robert Appleby2

  • 1IFOM, The AIRC Institute of Molecular Oncology, Milan, Italy.

Molecular Cell
|August 23, 2024
PubMed
Summary

DNA repair protein RAD51 protects against genomic instability by shielding abasic sites, preventing DNA breaks during replication. This is crucial for maintaining genome integrity when DNA damage occurs.

Keywords:
APOBEC3BBRCA2DNA recombinationDNA replicationDNMT1RAD51TET2abasic sitesbase excision repairreplication fork protection

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Area of Science:

  • Molecular Biology
  • Genomics
  • DNA Repair Mechanisms

Background:

  • Abasic sites are common DNA lesions arising from base modifications.
  • Unrepaired abasic sites in single-stranded DNA (ssDNA) pose a risk of chromosomal breakage during replication.
  • The mechanisms preventing abasic DNA rupture and subsequent genomic instability are not fully understood.

Purpose of the Study:

  • To elucidate the role of RAD51 in protecting abasic sites.
  • To understand how abasic site cleavage is prevented during DNA replication.
  • To investigate the contribution of BRCA2 and RAD51 to genomic stability in the context of abasic lesions.

Main Methods:

  • Cryo-electron microscopy (cryo-EM) to visualize protein-DNA interactions.
  • Xenopus laevis egg extracts and human cell lines for experimental models.
  • Assays to detect abasic site accumulation and DNA cleavage.

Main Results:

  • RAD51 nucleofilaments specifically recognize and bind to abasic sites, increasing their association rate with DNA.
  • Loss of BRCA2 or RAD51 leads to abasic site accumulation and sensitivity to APE1 cleavage.
  • RAD51 binding prevents MRE11-RAD50 complex-mediated cleavage of abasic DNA, suppressing replication fork breakage.

Conclusions:

  • RAD51 plays a critical protective role at abasic sites, preventing DNA breaks.
  • BRCA2 and RAD51 are essential for maintaining genomic stability against DNA base alterations.
  • This study reveals a key mechanism for safeguarding replicating DNA from unrepaired abasic lesions.