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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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Updated: Jan 18, 2026

Atomic Force Microscopy Investigations of DNA Lesion Recognition in Nucleotide Excision Repair
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The RecBC complex protects single-stranded DNA gaps during lesion bypass.

Gaëlle Philippin1, Pauline Dupaigne2, Élodie Chrabaszcz1

  • 1Cancer Research Center of Marseille: Team DNA Damage and Genome Instability|CNRS, Inserm, Institut Paoli-Calmettes, Aix Marseille Université, Marseille 13009, France.

Proceedings of the National Academy of Sciences of the United States of America
|September 10, 2025
PubMed
Summary
This summary is machine-generated.

The RecBC complex protects nascent DNA during replication, preventing degradation by nucleases like ExoI. This ensures efficient DNA lesion bypass through Translesion Synthesis or Homology Directed Gap Repair.

Keywords:
DNA damage toleranceDNA lesionRecBCsingle-stranded DNA gaptranslesion synthesis

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Area of Science:

  • Molecular Biology
  • Genetics
  • DNA Repair

Background:

  • DNA replication halts at unrepaired lesions, creating single-stranded DNA (ssDNA) gaps.
  • These gaps are repaired via Translesion Synthesis (TLS) or Homology Directed Gap Repair (HDGR).

Purpose of the Study:

  • To investigate a novel role for the RecBC complex in DNA lesion tolerance.
  • To understand how RecBC protects nascent DNA during replication restart.

Main Methods:

  • Genetic analysis of RecBC function in DNA lesion bypass.
  • Investigating the interaction between RecBC, ExoI, and nascent DNA.

Main Results:

  • RecBC protects nascent DNA from degradation by ExoI, independent of its catalytic activity and the RecD subunit.
  • RecBC is crucial for efficient TLS and HDGR, particularly at strong blocking lesions.
  • Loss of RecBC allows ExoI to degrade nascent DNA, impairing lesion tolerance.

Conclusions:

  • RecBC has a non-canonical role in safeguarding nascent DNA during replication restart.
  • This protective function is conserved across species, similar to BRCA2 in humans.
  • RecBC is essential for maintaining genome integrity following DNA damage.