Rad51-mediated replication fork reversal is a global response to genotoxic treatments in human cells
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...
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| Vydané v: | The Journal of cell biology Ročník 208; číslo 5; s. 563 |
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| Hlavní autori: | , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | English |
| Vydavateľské údaje: |
United States
02.03.2015
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| Predmet: | |
| ISSN: | 1540-8140, 1540-8140 |
| On-line prístup: | Zistit podrobnosti o prístupe |
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| Abstract | 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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| AbstractList | 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. 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.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. |
| Author | Mutreja, Karun Schmid, Jonas A Zellweger, Ralph Lopes, Massimo Berti, Matteo Dalcher, Damian Herrador, Raquel Vindigni, Alessandro |
| Author_xml | – sequence: 1 givenname: Ralph surname: Zellweger fullname: Zellweger, Ralph organization: Institute of Molecular Cancer Research, University of Zurich, 8057 Zurich, Switzerland – sequence: 2 givenname: Damian surname: Dalcher fullname: Dalcher, Damian organization: Institute of Molecular Cancer Research, University of Zurich, 8057 Zurich, Switzerland – sequence: 3 givenname: Karun surname: Mutreja fullname: Mutreja, Karun organization: Institute of Molecular Cancer Research, University of Zurich, 8057 Zurich, Switzerland – sequence: 4 givenname: Matteo surname: Berti fullname: Berti, Matteo organization: Department of Biochemistry and Molecular Biology, Saint Louis University School of Medicine, St. Louis, MO 63104 – sequence: 5 givenname: Jonas A surname: Schmid fullname: Schmid, Jonas A organization: Institute of Molecular Cancer Research, University of Zurich, 8057 Zurich, Switzerland – sequence: 6 givenname: Raquel surname: Herrador fullname: Herrador, Raquel organization: Institute of Molecular Cancer Research, University of Zurich, 8057 Zurich, Switzerland – sequence: 7 givenname: Alessandro surname: Vindigni fullname: Vindigni, Alessandro organization: Department of Biochemistry and Molecular Biology, Saint Louis University School of Medicine, St. Louis, MO 63104 – sequence: 8 givenname: Massimo surname: Lopes fullname: Lopes, Massimo email: lopes@imcr.uzh.ch organization: Institute of Molecular Cancer Research, University of Zurich, 8057 Zurich, Switzerland lopes@imcr.uzh.ch |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/25733714$$D View this record in MEDLINE/PubMed |
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| Snippet | Replication fork reversal protects forks from breakage after poisoning of Topoisomerase 1. We here investigated fork progression and chromosomal breakage in... |
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| SubjectTerms | Cell Line, Tumor DNA Damage DNA Replication HEK293 Cells Humans Poly(ADP-ribose) Polymerases - genetics Poly(ADP-ribose) Polymerases - metabolism Rad51 Recombinase - metabolism RecQ Helicases - genetics RecQ Helicases - metabolism Topoisomerase Inhibitors - toxicity |
| Title | Rad51-mediated replication fork reversal is a global response to genotoxic treatments in human cells |
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