ArticleProceedings of the National Academy of Sciences of the United States of America2005
Premature condensation induces breaks at the interface of early and late replicating chromosome bands bearing common fragile sites.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
59 citing papers in PubMed, 106 citations in OpenAlex.
- The Tale of the Guanosine Tract in Repeat Expansion Disorders.Molecular neurobiology · 2026Review
- Article
- Mistimed origin licensing and activation stabilize common fragile sites under tight DNA-replication checkpoint activation.Nature structural & molecular biology · 2023Article
- UBE2T resolves transcription-replication conflicts and protects common fragile sites in primordial germ cells.Cellular and molecular life sciences : CMLS · 2023Article
- Mitotic DNA synthesis in response to replication stress requires the sequential action of DNA polymerases zeta and delta in human cells.Nature communications · 2023Article
- Visualizing Active Replication Regions in S-Phase Chromosomes.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Applicability of Scoring Calyculin A-Induced Premature Chromosome Condensation Objects for Dose Assessment Including for Radiotherapy Patients.Cytogenetic and genome research · 2023Article
- Chemical-Induced Premature Chromosome Condensation Protocol.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Fragile sites, chromosomal lesions, tandem repeats, and disease.Frontiers in genetics · 2022Review
- Epigenomic signatures associated with spontaneous and replication stress-induced DNA double strand breaks.Frontiers in genetics · 2022Article
- Targeting the DNA Damage Response for Cancer Therapy by Inhibiting the Kinase Wee1.Frontiers in oncology · 2022Review
- Large Intronic Deletion of the Fragile Site GeneFrontiers in genetics · 2021Article
- Rebelled epigenome: histone H3S10 phosphorylation and H3S10 kinases in cancer biology and therapy.Clinical epigenetics · 2020Review
- Common Fragile Sites Are Characterized by Faulty Condensin Loading after Replication Stress.Cell reports · 2020Article
- Folate stress induces SLX1- and RAD51-dependent mitotic DNA synthesis at the fragile X locus in human cells.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Seq'ing identity and function in a repeat-derived noncoding RNA world.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2020Review
- Transcription-mediated organization of the replication initiation program across large genes sets common fragile sites genome-wide.Nature communications · 2019Article
- DNA-PKcs and ATM epistatically suppress DNA end resection and hyperactivation of ATR-dependent GScientific reports · 2019Article
- Mitotic CDK Promotes Replisome Disassembly, Fork Breakage, and Complex DNA Rearrangements.Molecular cell · 2019Article
- Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Various studies suggest a tight relationship between chromosome rearrangements driving tumor progression and breaks at loci called common fragile sites. Most of these sites are induced after perturbation of the replication dynamics, notably by aphidicolin treatment. We have mapped the majority of these sites to the interface of R and G bands, which calls into question the previous assignment of aphidicolin-sensitive sites to R bands. This observation suggests that most of them correspond to loci that ensure the transition between early and late replicating domains. We show that calyculin A, which triggers chromosome condensation at any phase of the cell cycle but does not markedly impair replication, induces damage in the chromosomes of human lymphocytes treated in G(2) but not in G(1) phase. We demonstrate that these lesions colocalize with those induced by aphidicolin treatment. Hence, common fragile site stability is compromised, whether aphidicolin delays replication or calyculin A advances condensation. We also show that, in cells that go through an unperturbed S phase, completion of their replication and/or replication-associated chromatin reorganization occur all along the G(2) phase, which may explain their inability to condense properly after calyculin A treatment during this phase of the cell cycle.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.