Collaboration and competition between DNA double‐strand break repair pathways
Open accessAbstract
DNA double‐strand breaks resulting from normal cellular processes including replication and exogenous sources such as ionizing radiation pose a serious risk to genome stability, and cells have evolved different mechanisms for their efficient repair. The two major pathways involved in the repair of double‐strand breaks in eukaryotic cells are non‐homologous end joining and homologous recombination. Numerous factors affect the decision to repair a double‐strand break via these pathways, and accumulating evidence suggests these major repair pathways both cooperate and compete with each other at double‐strand break sites to facilitate efficient repair and promote genomic integrity.
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It states that non-homologous end joining repairs the break in an error-prone manner and frequently leaves small insertions or deletions.
“The lesion can be healed by the error-prone Non-Homologous End-Joining (NHEJ) pathway, which often results in creation of an insertion/deletion (INDEL) of one to several bases7.”
From A high-fidelity Cas9 mutant delivered as a ribonucleoprotein complex enables efficient gene editing in human hematopoietic stem and progenitor cells (2018) · cites this paper as [7]
Section 4, “Repair by non-homologous end joining” (page not provided), says that processing DNA ends during NHEJ can produce insertions and deletions, making it more error-prone than homologous recombination. It does not establish that INDELs occur often or that they are typically one to several bases long. (LLM, conf=0.87)
Experimental — accuracy not yet measuredBRCA2 binds and loads RAD51, which mediates strand invasion of duplex DNA with homologous sequences.
“Subsequently, these DNA ends become competent for recombination when BRCA2 binds and loads RAD51, which mediates strand invasion of duplex DNA with homologous sequences [4].”
From Hereditary Breast Cancer and the BRCA1-Associated FANCJ/BACH1/BRIP1 (2011) · cites this paper as [4]
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References 94 · Cited by 326
- Authors
- Kass, E. M., & Jasin, M.
- Affiliations
- Memorial Sloan Kettering Cancer Center (US)
- Corresponding author
- Jasin, Maria
- ORCID
- Jasin, Maria
- Venue
- FEBS Letters
- Publisher
- Wiley
- Published
- 2010-08-04
- Volume
- 584
- Issue
- 17
- Pages
- 3703-3708
- ISSN
- 0014-5793 (ISSN-L)
- 1873-3468
- PMC
- PMC3954739
- OpenAlex
- W1972988800
- Semantic Scholar
- dd3f3bd9eb1ae75ff1e38fd912d889979e23b0b8
- Cited by
- 326
- References
- 94
- Citations by year
- 2026: 2 · 2025: 8 · 2024: 7 · 2023: 7 · 2022: 15 · 2021: 17 · 2020: 21 · 2019: 14 · 2018: 22 · 2017: 17 · 2016: 30 · 2015: 27 · 2014: 33 · 2013: 38 · 2012: 27
- FWCI
- 2.97
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- FEBS Letters (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (P01CA94060, R01GM54668)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Health Sciences › Medicine › Oncology › PARP inhibition in cancer therapy
- Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Effects of Radiation Exposure
- Keywords
- DNA double-strand break repair, non-homologous end joining, homologous recombination, genome stability, ionizing radiation, DNA repair pathways
- MeSH terms
- Animals, Base Sequence, Brain, Cell Cycle, DNA Damage, DNA Repair, DNA Replication, Fanconi Anemia, Homeostasis, Humans, Mutation, Recombination, Genetic, Saccharomyces cerevisiae, Conserved Sequence, Genes, BRCA1, Genes, BRCA2, DNA Breaks, Double-Stranded
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