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Updated: Jan 18, 2026

Atomic Force Microscopy Investigations of DNA Lesion Recognition in Nucleotide Excision Repair
Published on: May 24, 2017
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.
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.
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.
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