The DOI matches its Crossref record; 60 of the 60 references it cites were found in a registry or an index.
Rad51-mediated replication fork reversal is a global response to genotoxic treatments in human cells
Open accessAbstract
Replication fork reversal protects forks from breakage after poisoning of Topoisomerase 1. We here investigated fork progression and chromosomal breakage in human cells in response to a panel of sublethal genotoxic treatments, using other topoisomerase poisons, DNA synthesis inhibitors, interstrand cross-linking inducers, and base-damaging agents. We used electron microscopy to visualize fork architecture under these conditions and analyzed the association of specific molecular features with checkpoint activation. Our data identify replication fork uncoupling and reversal as global responses to genotoxic treatments. Both events are frequent even after mild treatments that do not affect fork integrity, nor activate checkpoints. Fork reversal was found to be dependent on the central homologous recombination factor RAD51, which is consistently present at replication forks independently of their breakage, and to be antagonized by poly (ADP-ribose) polymerase/RECQ1-regulated restart. Our work establishes remodeling of uncoupled forks as a pivotal RAD51-regulated response to genotoxic stress in human cells and as a promising target to potentiate cancer chemotherapy.
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Cites
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The multifaceted roles of PARP1 in DNA repair and chromatin remodelling
Ray Chaudhuri, A., & Nussenzweig, A. (2017) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm.2017.53 · Cited by 1,786
DNA double-strand break repair-pathway choice in somatic mammalian cells
Scully, R., Panday, A., Elango, R., & Willis, N. A. (2019) · Nature Reviews Molecular Cell Biology · doi:10.1038/s41580-019-0152-0 · Cited by 1,457
High speed of fork progression induces DNA replication stress and genomic instability
Maya-Mendoza, A., Moudry, P., Merchut-Maya, J. M., Lee, M., Strauss, R., & Bartek, J. (2018) · Nature · doi:10.1038/s41586-018-0261-5 · Cited by 514
Mechanisms of Oncogene-Induced Replication Stress: Jigsaw Falling into Place
Kotsantis, P., Petermann, E., & Boulton, S. J. (2018) · Cancer Discovery · doi:10.1158/2159-8290.cd-17-1461 · Cited by 416
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Metadata
- Authors
- Zellweger, R., Dalcher, D., Mutreja, K., Berti, M., Schmid, J. A., Herrador, R., Vindigni, A., & Lopes, M.
- Venue
- Journal of Cell Biology
- Publisher
- Rockefeller University Press
- Published
- 2015-03-02
- Volume
- 208
- Issue
- 5
- Pages
- 563-579
- ISSN
- 0021-9525 (ISSN-L)
- 1540-8140
- OpenAlex
- W2104584181
- Cited by
- 677
- References
- 60
- FWCI
- 23.41
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- CoChat. (2026). Citation check: Rad51-mediated replication fork reversal is a global response to genotoxic treatments in human cells. https://app.cochat.ai/papers/10.1083/jcb.201406099
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- Zellweger, R., Dalcher, D., Mutreja, K., Berti, M., Schmid, J. A., Herrador, R., Vindigni, A., & Lopes, M. (2015). Rad51-mediated replication fork reversal is a global response to genotoxic treatments in human cells. Journal of Cell Biology. https://doi.org/10.1083/jcb.201406099
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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