ArticleNature structural & molecular biology2019
Transcription-dependent regulation of replication dynamics modulates genome stability.
Article in Nature structural & molecular biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
57 citing papers in PubMed, 107 citations in OpenAlex.
- 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
- Transcription elongation can be sufficient, but is not necessary, to advance replication timing.EMBO reports · 2026Article
- Transcription at an inducible common fragile site reveals replication origin strength hierarchy.Nucleic acids research · 2026Article
- Multiple strategies to resolve the conflict between replication and transcription in mammalian cells.Nucleic acids research · 2026Article
- Master transcription-factor binding sites constitute the core of early replication control elements.The EMBO journal · 2025Article
- DNA replication timing reveals genome-wide features of transcription and fragility.Nature communications · 2025Article
- The double life of mammalian DNA replication origins.Genes & development · 2025Review
- Transcription can be sufficient, but is not necessary, to advance replication timing.bioRxiv : the preprint server for biology · 2025Article
- Replication stress induces POLQ-mediated structural variant formation throughout common fragile sites after entry into mitosis.Nature communications · 2024Article
- Histone variant macroH2A1 regulates synchronous firing of replication origins in the inactive X chromosome.Nucleic acids research · 2024Article
- Genome-wide identification of replication fork stalling/pausing sites and the interplay between RNA Pol II transcription and DNA replication progression.Genome biology · 2024Article
- Linear interaction between replication and transcription shapes DNA break dynamics at recurrent DNA break Clusters.Nature communications · 2024Article
- Insights into common fragile site instability: DNA replication challenges at DNA repeat sequences.Emerging topics in life sciences · 2023Article
- RIF1 regulates early replication timing in murine B cells.Nature communications · 2023Article
- Transcription-Replication Conflicts as a Source of Genome Instability.Annual review of genetics · 2023Review
- RNAPII-dependent ATM signaling at collisions with replication forks.Nature communications · 2023Article
- Replication stress causes delayed mitotic entry and chromosome 12 fragility at the ANKS1B large neuronal gene in human induced pluripotent stem cells.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2023Article
- Mistimed origin licensing and activation stabilize common fragile sites under tight DNA-replication checkpoint activation.Nature structural & molecular biology · 2023Article
- Replication timing and transcriptional control: beyond cause and effect - part IV.Current opinion in genetics & development · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Common fragile sites (CFSs) are loci that are hypersensitive to replication stress and hotspots for chromosomal rearrangements in cancers. CFSs replicate late in S phase, are cell-type specific and nest in large genes. The relative impact of transcription-replication conflicts versus a low density in initiation events on fragility is currently debated. Here we addressed the relationships between transcription, replication, and instability by manipulating the transcription of endogenous large genes in chicken and human cells. We found that inducing low transcription with a weak promoter destabilized large genes, whereas stimulating their transcription with strong promoters alleviated instability. Notably, strong promoters triggered a switch to an earlier replication timing, supporting a model in which high transcription levels give cells more time to complete replication before mitosis. Transcription could therefore contribute to maintaining genome integrity, challenging the dominant view that it is exclusively a threat.
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What OpenQuestion holds
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.