ArticleBMC biology2014
Checkpoint-independent scaling of the Saccharomyces cerevisiae DNA replication program.
Article in BMC biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed, 12 citations in OpenAlex.
- Stimulation of adaptive gene amplification by origin firing under replication fork constraint.Nucleic acids research · 2022Article
- Histones on fire: the effect of Dun1 and Mrc1 on origin firing and replication of hyper-acetylated genomes.Current genetics · 2021Review
- Review
- Genomic methods for measuring DNA replication dynamics.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2020Review
- Mrc1/Claspin: a new role for regulation of origin firing.Current genetics · 2017Review
- Cell-to-cell variability and robustness in S-phase duration from genome replication kinetics.Nucleic acids research · 2017Article
- Checkpoint-Independent Regulation of Origin Firing by Mrc1 through Interaction with Hsk1 Kinase.Molecular and cellular biology · 2017Article
- Model-based analysis of DNA replication profiles: predicting replication fork velocity and initiation rate by profiling free-cycling cells.Genome research · 2017Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIn budding yeast, perturbations that prolong S phase lead to a proportionate delay in the activation times of most origins. The DNA replication checkpoint was implicated in this scaling phenotype, as an intact checkpoint was shown to be required for the delayed activation of late origins in response to hydroxyurea treatment. In support of that, scaling is lost in cells deleted of mrc1, a mediator of the replication checkpoint signal. Mrc1p, however, also plays a role in normal replication.
resultsTo examine whether the replication checkpoint is required for scaling the replication profile with S phase duration we measured the genome-wide replication profile of different MRC1 alleles that separate its checkpoint function from its role in normal replication, and further analyzed the replication profiles of S phase mutants that are checkpoint deficient. We found that the checkpoint is not required for scaling; rather the unique replication phenotype of mrc1 deleted cells is attributed to the role of Mrc1 in normal replication. This is further supported by the replication profiles of tof1Δ which functions together with Mrc1p in normal replication, and by the distinct replication profiles of specific POL2 alleles which differ in their interaction with Mrc1p.
conclusionsWe suggest that the slow fork progression in mrc1 deleted cells reduces the likelihood of passive replication leading to the activation of origins that remain mostly dormant in wild-type cells.
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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.