Evidence map›Paper›PMID 15805465›Full record

ArticleGenes & development2005

Replication checkpoint kinase Cds1 regulates Mus81 to preserve genome integrity during replication stress.

Mihoko Kai, Michael N Boddy, Paul Russell, Teresa S-F Wang

Open access · diamondAbstract readComparative Study
In one paragraph

Article in Genes & development, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.

0numbers the graph read from it
0cells of the map it votes in
75citing 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

75 citing papers in PubMed, 140 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. The intra-S phase checkpoint directly regulates replication elongation to preserve the integrity of stalled replisomes.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  10. Making Choices: DNA Replication Fork Recovery Mechanisms.Seminars in cell & developmental biology · 2021
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Replication fork stalling elicits chromatin compaction for the stability of stalling replication forks.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  20. Review

15 more citing papers are in PubMed but not listed here.

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 1 country.

Mihoko KaiDepartment of Pathology, Stanford University School of Medicine, Stanford, California 94305-5324, USA.
Michael N Boddy
Paul Russell
Teresa S-F Wang
Scripps Research Institute · US

Funding

Studies of the DNA Replication CheckpointR01GM059447 · NIGMS · SCRIPPS RESEARCH INSTITUTE, THE · PI RUSSELL, PAUL · 1999 to 2016
$6.0M
CONTROL OF DNA REPLICATION AND CELL DIVISIONR01CA054415 · NCI · STANFORD UNIVERSITY · PI WANG, TERESA S · 1991 to 2007
$2.5M
NCI NIH HHS CA54415NCI NIH HHS R01 CA054415NIGMS NIH HHS GM059447NIGMS NIH HHS R01 GM059447
6 · The paper itself

Abstract

The replication checkpoint kinase Cds1 preserves genome integrity by stabilizing stalled replication forks. Cds1 targets substrates through its FHA domain. The Cds1 FHA domain interacts with Mus81, a subunit of the Mus81-Eme1 structure-specific endonuclease. We report here that Mus81 and Rhp51 are required for generating deletion mutations in fission yeast replication mutants that experience replication stress. A mutation in the Mus81 FHA-binding motif eliminates its Cds1-binding and Cds1-dependent phosphorylation. Furthermore, this mutation exacerbates the deletion mutator phenotype of a replication mutant, and induces a hyper-recombination phenotype in hydroxyurea-treated cells. In unperturbed cells, Mus81 associates with chromatin throughout S phase. In replication mutants grown at semipermissive temperature, Mus81 undergoes minor Cds1-dependent phosphorylation, remains chromatin-associated, generates deletion mutations, and maintains cell growth. Upon S-phase arrest by acute hydroxyurea treatment, Mus81 is not required for cell viability but is essential for recovery from replication fork collapse. Moreover, Mus81 undergoes extensive Cds1-dependent phosphorylation and dissociates from chromatin in hydroxyurea-arrested cells, thereby preventing it from cleaving stalled replication forks that could lead to fork breakage and chromosomal rearrangement. These results provide novel insights into how Cds1 regulates Mus81 accordingly when cells experience different replication stress to preserve genome integrity.

Indexed as

Checkpoint Kinase 2ChromatinDNA-Binding ProteinsDNA PrimersDNA ReplicationEndonucleasesGenomic InstabilityHydroxyureaMutationPhosphorylationProtein Serine-Threonine KinasesRad51 RecombinaseRecombination, GeneticSchizosaccharomycesSchizosaccharomyces pombe ProteinsS PhaseCds1 protein, S pombeCheckpoint Kinase 2ChromatinDNA-Binding ProteinsDNA PrimersEndonucleasesHydroxyureaMUS81 protein, S pombeProtein Serine-Threonine KinasesRad51 RecombinaseRHP51 protein, S pombeSchizosaccharomyces pombe Proteins

Identifiers

PMID15805465
PMCPMC1080131
OpenAlexW1993567700

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.