ArticleThe Journal of biological chemistry2010
Relicensing of transcriptionally inactivated replication origins in budding yeast.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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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.
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Who cites it
24 citing papers in PubMed, 38 citations in OpenAlex.
- A lethal ORC ATPase mutation is suppressed by alterations in ORC and RNA Pol II transcription components.PloS one · 2026Article
- Review
- Replication stress generates distinctive landscapes of DNA copy number alterations and chromosome scale losses.Genome biology · 2022Article
- Mobile origin-licensing factors confer resistance to conflicts with RNA polymerase.Cell reports · 2022Article
- Locus-specific transcription silencing at the FHIT gene suppresses replication stress-induced copy number variant formation and associated replication delay.Nucleic acids research · 2021Article
- Transcription shapes DNA replication initiation to preserve genome integrity.Genome biology · 2021Article
- Genome-wide high-resolution mapping of mitotic DNA synthesis sites and common fragile sites by direct sequencing.Cell research · 2020Article
- Sir2 takes affirmative action to ensure equal opportunity in replication origin licensing.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Transcription-mediated replication hindrance: a major driver of genome instability.Genes & development · 2019Review
- Dynamics of DNA replication in a eukaryotic cell.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Transcription-dependent regulation of replication dynamics modulates genome stability.Nature structural & molecular biology · 2019Article
- Article
- Noncoding transcription influences the replication initiation program through chromatin regulation.Genome research · 2018Article
- The Protective Role of Dormant Origins in Response to Replicative Stress.International journal of molecular sciences · 2018Review
- FANCD2 binding identifies conserved fragile sites at large transcribed genes in avian cells.Nucleic acids research · 2018Article
- Fragile sites in cancer: more than meets the eye.Nature reviews. Cancer · 2017Review
- Rescue from replication stress during mitosis.Cell cycle (Georgetown, Tex.) · 2017Review
- Transcription-replication conflicts at chromosomal fragile sites-consequences in M phase and beyond.Chromosoma · 2017Review
- Recruitment of Fkh1 to replication origins requires precisely positioned Fkh1/2 binding sites and concurrent assembly of the pre-replicative complex.PLoS genetics · 2017Article
- Eukaryotic replication origins: Strength in flexibility.Nucleus (Austin, Tex.) · 2016Review
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
DNA replication origins are licensed in early G(1) phase of the cell cycle where the origin recognition complex (ORC) recruits the minichromosome maintenance (MCM) helicase to origins. These pre-replicative complexes (pre-RCs) remain inactive until replication is initiated in the S phase. However, transcriptional activity in the regions of origins can eliminate their functionality by displacing the components of pre-RC from DNA. We analyzed genome-wide data of mRNA and cryptic unstable transcripts in the context of locations of replication origins in yeast genome and found that at least one-third of the origins are transcribed and therefore might be inactivated by transcription. When investigating the fate of transcriptionally inactivated origins, we found that replication origins were repetitively licensed in G(1) to reestablish their functionality after transcription. We propose that reloading of pre-RC components in G(1) might be utilized for the maintenance of sufficient number of competent origins for efficient initiation of DNA replication in S phase.
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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.