ArticleNature communications2019
Transcription-mediated organization of the replication initiation program across large genes sets common fragile sites genome-wide.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.
What it found
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
73 citing papers in PubMed, 107 citations in OpenAlex.
- Single-cell mapping of chromosome breaks identifies multiple fragile site classes with distinct DNA replication timing landscapes.Nature communications · 2026Article
- Replication stress in cancer: origins, consequences and therapeutic opportunities.Nature reviews. Cancer · 2026Review
- Article
- ERCC6 at the Transcription-Replication Interface: Integration of Transcription-Coupled Repair with Replication Stress Responses.International journal of molecular sciences · 2026Review
- Multiomic characterization of DNA released after airway exposure to allergens and nanoparticles reveals selective export of repetitive and fragile site DNA.Physiological genomics · 2026Article
- Determinants of dicentric chromosome breakage inbioRxiv : the preprint server for biology · 2026Article
- Replication origin flexibility: a tool to mitigate the hazards of excess replication.Trends in genetics : TIG · 2026Review
- Recurrent DNA break clusters drive replication-stress-induced copy number variants and genome diversification.Nature communications · 2026Article
- ATR and TopBP1 oppose to control dormant origin activity and global replication dynamics, providing a first defense against replication stress.Nucleic acids research · 2026Article
- Transcription at an inducible common fragile site reveals replication origin strength hierarchy.Nucleic acids research · 2026Article
- DNA shape and epigenomics distinguish the mechanistic origin of human genomic structural variations.Nucleic acids research · 2025Article
- DNA replication initiation timing is important for maintaining genome integrity.Journal of bacteriology · 2025Article
- Single cell multiomics approach to analyze replication timing and gene expression in mouse preimplantation embryos.Communications biology · 2025Article
- DNA replication timing reveals genome-wide features of transcription and fragility.Nature communications · 2025Article
- The fork protection complex generates DNA topological stress-induced DNA damage while ensuring full and faithful genome duplication.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Culture-acquired genetic variation in human pluripotent stem cells: Twenty years on.BioEssays : news and reviews in molecular, cellular and developmental biology · 2024Review
- Replication stress induces POLQ-mediated structural variant formation throughout common fragile sites after entry into mitosis.Nature communications · 2024Article
- Replication fork stalling in late S-phase elicits nascent strand degradation by DNA mismatch repair.Nucleic acids research · 2024Article
- FANCD2 genome binding is nonrandom and is enriched at large transcriptionally active neural genes prone to copy number variation.Functional & integrative genomics · 2024Article
- A post-irradiation-induced replication stress promotes RET proto-oncogene breakage.European thyroid journal · 2024Article
13 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Common fragile sites (CFSs) are chromosome regions prone to breakage upon replication stress known to drive chromosome rearrangements during oncogenesis. Most CFSs nest in large expressed genes, suggesting that transcription could elicit their instability; however, the underlying mechanisms remain elusive. Genome-wide replication timing analyses here show that stress-induced delayed/under-replication is the hallmark of CFSs. Extensive genome-wide analyses of nascent transcripts, replication origin positioning and fork directionality reveal that 80% of CFSs nest in large transcribed domains poor in initiation events, replicated by long-travelling forks. Forks that travel long in late S phase explains CFS replication features, whereas formation of sequence-dependent fork barriers or head-on transcription-replication conflicts do not. We further show that transcription inhibition during S phase, which suppresses transcription-replication encounters and prevents origin resetting, could not rescue CFS stability. Altogether, our results show that transcription-dependent suppression of initiation events delays replication of large gene bodies, committing them to instability.
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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.