ArticleMolecular cell2015
Post-licensing Specification of Eukaryotic Replication Origins by Facilitated Mcm2-7 Sliding along DNA.
Article in Molecular cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 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
86 citing papers in PubMed, 134 citations in OpenAlex.
- MCM2-7 proteins promote NF-κB transcriptional activity through cooperative promoter recruitment.Bioscience reports · 2026Article
- Polymerase face-off: emerging concepts in transcription-replication coordination.EMBO reports · 2026Review
- Slow RNAPII elongation enhances naive pluripotency rewiring while maintaining high replication fork speed.Science advances · 2026Article
- Transcription at an inducible common fragile site reveals replication origin strength hierarchy.Nucleic acids research · 2026Article
- A lethal ORC ATPase mutation is suppressed by alterations in ORC and RNA Pol II transcription components.PloS one · 2026Article
- Compact Origins and Where to Find Them: ORC's Guide to Genome-Wide Licensing.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025Review
- Senataxin prevents replicative stress induced by the Myc oncogene.Cell death & disease · 2025Article
- DNA replication recruits a friend to overcome a challenging break-up.The EMBO journal · 2024Article
- MCM2-7 loading-dependent ORC release ensures genome-wide origin licensing.Nature communications · 2024Article
- MCM8 interacts with DDX5 to promote R-loop resolution.The EMBO journal · 2024Article
- Dormant origin firing promotes head-on transcription-replication conflicts at transcription termination sites in response to BRCA2 deficiency.Nature communications · 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
- The MCM2-7 Complex: Roles beyond DNA Unwinding.Biology · 2024Review
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- Quantity and quality of minichromosome maintenance protein complexes couple replication licensing to genome integrity.Communications biology · 2024Review
- Identification of 1600 replication origins ineLife · 2024Article
- The Origin Recognition Complex: From Origin Selection to Replication Licensing in Yeast and Humans.Biology · 2023Review
- RIF1 regulates early replication timing in murine B cells.Nature communications · 2023Article
- Where and when to start: Regulating DNA replication origin activity in eukaryotic genomes.Nucleus (Austin, Tex.) · 2023Review
26 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Eukaryotic genomes are replicated from many origin sites that are licensed by the loading of the replicative DNA helicase, Mcm2-7. How eukaryotic origin positions are specified remains elusive. Here we show that, contrary to the bacterial paradigm, eukaryotic replication origins are not irrevocably defined by selection of the helicase loading site, but can shift in position after helicase loading. Using purified proteins we show that DNA translocases, including RNA polymerase, can push budding yeast Mcm2-7 double hexamers along DNA. Displaced Mcm2-7 double hexamers support DNA replication initiation distal to the loading site in vitro. Similarly, in yeast cells that are defective for transcription termination, collisions with RNA polymerase induce a redistribution of Mcm2-7 complexes along the chromosomes, resulting in a corresponding shift in DNA replication initiation sites. These results reveal a eukaryotic origin specification mechanism that departs from the classical replicon model, helping eukaryotic cells to negotiate transcription-replication conflict.
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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.