ArticleCell reports2025
Distinct roles of the two BRCA2 DNA-binding domains in DNA damage repair and replication fork preservation.
Article in Cell reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed.
- The eukaryotic homology search complex distorts donor DNA structure to probe for homology.Genes & development · 2026Article
- Multifaceted roles of PDS5B in RAD51-dependent homology-directed DNA repair and replication fork protection.Nature communications · 2026Article
- RCC1 knockdown sensitizes drug-resistant colorectal cancer to 5-fluorouracil or doxorubicin by impairing DNA repair.Cancer drug resistance (Alhambra, Calif.) · 2025Article
- Liver fibrosis in biliary atresia: identification of the key gene EDIL3 via integrated bioinformatics.Frontiers in medicine · 2025Article
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Abstract
Homologous recombination (HR) removes DNA double-strand breaks (DSBs) and preserves stressed DNA replication forks. Successful HR execution requires the tumor suppressor BRCA2, which harbors distinct DNA-binding domains (DBDs): one that possesses three oligonucleotide/oligosaccharide-binding (OB) folds (OB-DBD) and another residing in the C-terminal recombinase binding domain (CTRB-DBD). Here, we employ multi-faceted approaches to delineate the contributions of these domains toward HR and replication fork maintenance. We show that OB-DBD and CTRB-DBD confer single-strand DNA (ssDNA)- and dsDNA-binding capabilities, respectively, and that BRCA2 variants mutated in either domain are impaired in their ability to load the recombinase RAD51 onto ssDNA pre-occupied by RPA. While the CTRB-DBD mutant is modestly affected by DNA break repair, it exhibits a strong defect in the protection of stressed replication forks. In contrast, the OB-DBD is indispensable for both BRCA2 functions. Our study thus defines the unique contributions of the two BRCA2 DBDs in genome maintenance.
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