RAD51 is involved in repair of damage associated with DNA replication in mammalian cells

Lundin, Cecilia; Schultz, Niklas; Arnaudeau, Catherine; Mohindra, Atul; Hansen, Lasse Tengbjerg; Helleday, Thomas

doi:10.1016/s0022-2836(03)00313-9

Cited by 113DNA Repair MechanismsEffects of Radiation ExposurePARP inhibition in cancer therapy

RAD51 is involved in repair of damage associated with DNA replication in mammalian cells

Lundin, Cecilia, Schultz, Niklas, Arnaudeau, Catherine, Mohindra, Atul, Hansen, Lasse Tengbjerg, Helleday, Thomas·2003·Journal of Molecular Biology

DOI 10.1016/s0022-2836(03)00313-9

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Abstract

The RAD51 protein, a eukaryotic homologue of the Escherichia coli RecA protein, plays an important role in the repair of DNA double-strand breaks (DSBs) by homologous recombination (HR) in mammalian cells. Recent findings suggest that HR may be important in repair following replication arrest in mammalian cells. Here, we have investigated the role of RAD51 in the repair of different types of damage induced during DNA replication with etoposide, hydroxyurea or thymidine. We show that etoposide induces DSBs at newly replicated DNA more frequently than gamma-rays, and that these DSBs are different from those induced by hydroxyurea. No DSB was found following treatment with thymidine. Although these compounds appear to induce different DNA lesions during DNA replication, we show that a cell line overexpressing RAD51 is resistant to all of them, indicating that RAD51 is involved in repair of a wide range of DNA lesions during DNA replication. We observe fewer etoposide-induced DSBs in RAD51-overexpressing cells and that HR repair of etoposide-induced DSBs is faster. Finally, we show that induced long-tract HR in the hprt gene is suppressed in RAD51-overexpressing cells, although global HR appears not to be suppressed. This suggests that overexpression of RAD51 prevents long-tract HR occurring during DNA replication. We discuss our results in light of recent models suggested for HR at stalled replication forks.

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“Besides BRCA1, BRCA2, and Rad51 are also required for HR-mediated DNA repair and replication fork maintenance [25, 26].”
From NER initiation factors, DDB2 and XPC, regulate UV radiation response by recruiting ATR and ATM kinases to DNA damage sites (2013) · cites this paper as [25]
BRCA1, BRCA2, and Rad51 participate in HR-mediated DNA repair and replication fork maintenance.
“BRCA1, BRCA2, and Rad51 are known to participate in HR-mediated DNA repair and replication fork maintenance [25, 26].”
From NER initiation factors, DDB2 and XPC, regulate UV radiation response by recruiting ATR and ATM kinases to DNA damage sites (2013) · cites this paper as [25]

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Overexpression of KLF5 is associated with poor survival and G1/S progression in pancreatic cancer
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Mitochondrial superoxide contributes to oxidative stress exacerbated by DNA damage response in RAD51-depleted ovarian cancer cells
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Non-homologous end joining is the responsible pathway for the repair of fludarabine-induced DNA double strand breaks in mammalian cells
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Time-resolved RNA signatures of CD4+ T cells in Parkinson’s disease
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Repression of DNA Repair Mechanisms in IRF-4-Expressing and HTLV-I-Infected T Lymphocytes
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Gene Targeting Without DSB Induction Is Inefficient in Barley
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The analysis of S. cerevisiae cells deleted for mitotic cyclin Clb2 reveals a novel requirement of Sgs1 DNA helicase and Exonuclease 1 when replication forks break in the presence of alkylation damage
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Authors: Lundin, C., Schultz, N., Arnaudeau, C., Mohindra, A., Hansen, L. T., & Helleday, T.
Affiliations: Stockholm University (SE)
University of Sheffield (GB)
University of Copenhagen (DK)
Corresponding author: Helleday, Thomas
ORCID: Lundin, Cecilia
Helleday, Thomas
Venue: Journal of Molecular Biology
Publisher: Elsevier BV
Published: 2003-05
Volume: 328
Issue: 3
Pages: 521-535
ISSN: 0022-2836 (ISSN-L)
DOI: 10.1016/s0022-2836(03)00313-9
OpenAlex: W2052090116
Cited by: 113
References: 71
Citations by year: 2026: 1 · 2024: 4 · 2023: 3 · 2022: 2 · 2021: 3 · 2020: 2 · 2019: 2 · 2018: 3 · 2017: 4 · 2016: 4 · 2015: 8 · 2014: 4 · 2013: 5 · 2012: 4
FWCI: 3.79
Type: journal article
Language: en
Open access: closed
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Journal of Molecular Biology (publishedVersion)
PubMed (publishedVersion)
Funders: Stiftelsen Forska Utan Djurförsök
Cancerfonden
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Effects of Radiation Exposure
Health Sciences › Medicine › Oncology › PARP inhibition in cancer therapy
Keywords: RAD51, homologous recombination, DNA double-strand break repair, replication arrest, etoposide, hydroxyurea, thymidine, HPRT gene, stalled replication forks
MeSH terms: Animals, Cell Line, DNA Damage, DNA Repair, DNA Replication, DNA-Binding Proteins, Dose-Response Relationship, Drug, Etoposide, Cricetinae, Hydroxyurea, Hypoxanthine Phosphoribosyltransferase, Kinetics, Models, Genetic, Recombination, Genetic, Thymidine, Apoptosis, Rad51 Recombinase

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RAD51 is involved in repair of damage associated with DNA replication in mammalian cells

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