ArticleNucleic acids research2009
Transcription-associated recombination is independent of XRCC2 and mechanistically separate from homology-directed DNA double-strand break repair.
Article in Nucleic acids research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Heat shock factor 1 promotes proliferation and chemoresistance in diffuse large B-cell lymphoma by enhancing the cell cycle and DNA repair.Cell death & disease · 2025Article
- Fanconi anemia associated protein 20 (FAAP20) plays an essential role in homology-directed repair of DNA double-strand breaks.Communications biology · 2023Article
- WD repeat domain 5 promotes chemoresistance and Programmed Death-Ligand 1 expression in prostate cancer.Theranostics · 2021Article
- BRCA1 recruitment to transcriptional pause sites is required for R-loop-driven DNA damage repair.Molecular cell · 2015Article
- Transcription and recombination: when RNA meets DNA.Cold Spring Harbor perspectives in biology · 2014Review
- Interference between DNA replication and transcription as a cause of genomic instability.Current genomics · 2012Article
- Mechanisms of intron gain and loss in Drosophila.BMC evolutionary biology · 2011Article
- Transcription inhibition by DRB potentiates recombinational repair of UV lesions in mammalian cells.PloS one · 2011Article
- Article
- The S-phase checkpoint is required to respond to R-loops accumulated in THO mutants.Molecular and cellular biology · 2009Article
- Transcription and replication: breaking the rules of the road causes genomic instability.TranscriptionArticle
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
It has previously been shown that transcription greatly enhances recombination in mammalian cells. However, the proteins involved in catalysing this process and the recombination pathways involved in transcription-associated recombination (TAR) are still unknown. It is well established that both the BRCA2 protein and the RAD51 paralog protein XRCC2 are required for homologous recombination. Here, we show that the BRCA2 protein is also required for TAR, while the XRCC2 protein is not involved. Expression of the XRCC2 gene in XRCC2 mutated irs1 cells restores the defect in homologous recombination repair of an I-SceI-induced DNA double-strand break, while TAR is unaffected. Interestingly, the XRCC2-deficient irs1 cells are also proficient in recombination induced at slowed replication forks, suggesting that TAR is mechanistically linked with this recombination pathway. In conclusion, we show that TAR depends on BRCA2 but is independent of XRCC2, and that this recombination pathway is separate from that used to repair a two-ended DNA double-strand break.
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