Evidence map›Paper›PMID 15716375›Full record

ArticleThe Journal of cell biology2005

Temporal separation of replication and recombination requires the intra-S checkpoint.

Peter Meister, Angela Taddei, Laurence Vernis, Mickaël Poidevin, Susan M Gasser, Giuseppe Baldacci

Abstract read
In one paragraph

Article in The Journal of cell biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
–field-weighted citation impact
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

48 citing papers in PubMed.

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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

6 authors.

Peter MeisterCNRS UMR2027, Institut Curie, Centre Universitaire, 91405 Orsay Cedex, France.
Angela Taddei
Laurence Vernis
Mickaël Poidevin
Susan M Gasser
Giuseppe Baldacci

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In response to DNA damage and replication pausing, eukaryotes activate checkpoint pathways that prevent genomic instability by coordinating cell cycle progression with DNA repair. The intra-S-phase checkpoint has been proposed to protect stalled replication forks from pathological rearrangements that could result from unscheduled recombination. On the other hand, recombination may be needed to cope with either stalled forks or double-strand breaks resulting from hydroxyurea treatment. We have exploited fission yeast to elucidate the relationship between replication fork stalling, loading of replication and recombination proteins onto DNA, and the intra-S checkpoint. Here, we show that a functional recombination machinery is not essential for recovery from replication fork arrest and instead can lead to nonfunctional fork structures. We find that Rad22-containing foci are rare in S-phase cells, but peak in G2 phase cells after a perturbed S phase. Importantly, we find that the intra-S checkpoint is necessary to avoid aberrant strand-exchange events during a hydroxyurea block.

Indexed as

Cell SurvivalDNA-Binding ProteinsDNA DamageDNA RepairDNA ReplicationElectrophoresis, Gel, Two-DimensionalG2 PhaseGenomic InstabilityHydroxyureaRecombination, GeneticSchizosaccharomycesSchizosaccharomyces pombe ProteinsS PhaseDNA-Binding ProteinsHydroxyurearad52 protein, S pombeSchizosaccharomyces pombe Proteins

Identifiers

PMID15716375
PMCPMC2171758

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.