Evidence map›Paper›PMID 19273851›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2009

Recombination at DNA replication fork barriers is not universal and is differentially regulated by Swi1.

David W Pryce, Soshila Ramayah, Alessa Jaendling, Ramsay J McFarlane

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.0field-weighted citation impact, top 14% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

23 citing papers in PubMed, 34 citations in OpenAlex.

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  7. Timeless protection of telomeres.Current genetics · 2016
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 2 countries.

David W PryceNorth West Cancer Research Fund Institute, School of Biological Sciences, College of Natural Sciences, Bangor University, Bangor, Gwynedd, LL57 2UW, United Kingdom.
Soshila Ramayah
Alessa Jaendling
Ramsay J McFarlane
Bangor University · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

DNA replication stress has been implicated in the etiology of genetic diseases, including cancers. It has been proposed that genomic sites that inhibit or slow DNA replication fork progression possess recombination hotspot activity and can form potential fragile sites. Here we used the fission yeast, Schizosaccharomyces pombe, to demonstrate that hotspot activity is not a universal feature of replication fork barriers (RFBs), and we propose that most sites within the genome that form RFBs do not have recombination hotspot activity under nonstressed conditions. We further demonstrate that Swi1, the TIMELESS homologue, differentially controls the recombination potential of RFBs, switching between being a suppressor and an activator of recombination in a site-specific fashion.

Indexed as

DNA ReplicationCell Cycle ProteinsDNA-Binding ProteinsModels, GeneticRecombination, GeneticRegulatory Sequences, Nucleic AcidSchizosaccharomycesSchizosaccharomyces pombe ProteinsCell Cycle ProteinsDNA-Binding ProteinsSchizosaccharomyces pombe Proteinsswi1 protein, S pombe

Identifiers

PMID19273851
PMCPMC2660728
OpenAlexW2053209286

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.