Evidence map›Paper›PMID 27488803›Full record

ArticleCurrent genetics2017

A role for the spindle assembly checkpoint in the DNA damage response.

Roger Palou, Gloria Palou, David G Quintana

Open access · hybridAbstract read
In one paragraph

Article in Current genetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.6field-weighted citation impact, top 8% 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

31 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
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  6. Pak2 reduction induces a failure of early embryonic development in mice.Reproductive biology and endocrinology : RB&E · 2021
    Article
  7. Article
  8. Review
  9. Review
  10. PP2AJournal of cell science · 2020
    Article
  11. Checkpoint Responses to DNA Double-Strand Breaks.Annual review of biochemistry · 2020
    Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Review
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

3 authors at 1 institution in 1 country.

Roger PalouBiophysics Unit, School of Medicine, and Department of Biochemistry and Molecular Biology, Universitat Autonoma de Barcelona, Bellaterra, 08193, Catalonia, Spain.
Gloria PalouBiophysics Unit, School of Medicine, and Department of Biochemistry and Molecular Biology, Universitat Autonoma de Barcelona, Bellaterra, 08193, Catalonia, Spain.
David G QuintanaBiophysics Unit, School of Medicine, and Department of Biochemistry and Molecular Biology, Universitat Autonoma de Barcelona, Bellaterra, 08193, Catalonia, Spain. davidg.quintana@uab.cat.
Universitat Autònoma de Barcelona · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Spontaneous DNA damage poses a continuous threat to genomic integrity. If unchecked, genotoxic insults result in genomic instability, a hallmark of cancer cells. In eukaryotic cells a DNA Damage Response (DDR) detects and responds to genotoxic stress, acting as an anti-cancer barrier in humans. Among other actions, the DDR blocks the segregation of incompletely replicated or damaged chromosomes, thus preventing aneuploidy. In a work aimed at better understanding such S-M control, we recently showed that cells block anaphase through different control pathways. The S phase checkpoint kinase Mec1/ATR inhibits mitotic Cyclin Dependent Kinase activity through effector kinases Swe1/Wee1 and Rad53/Chk2. Cells also stabilize the levels of Pds1/securin to block sister chromatid segregation in response to DNA damage. We show here that Pds1/securin abundance is still secured when the S phase checkpoint response is fully abrogated in mec1/ATR tel1/ATM double null mutants. When such cells are exposed to genotoxic stress, Pds1/securin is stabilized in a spindle assembly checkpoint (SAC) dependent manner. Disruption of the SAC and the S phase checkpoint together, allows chromosome segregation in the presence of DNA damage or replication stress. Our results place the SAC as a part of the DDR, which appears to count on different, independent control layers to preserve genomic integrity when chromosome replication is challenged.

Indexed as

DNA DamageAnaphaseCDC2 Protein KinaseCell Cycle ProteinsCheckpoint Kinase 2Chromosome SegregationDNA, FungalHumansIntracellular Signaling Peptides and ProteinsModels, GeneticMutationProtein Serine-Threonine KinasesSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsSecurinS Phase Cell Cycle CheckpointsCDC2 Protein KinaseCell Cycle ProteinsCheckpoint Kinase 2DNA, FungalIntracellular Signaling Peptides and ProteinsMEC1 protein, S cerevisiaePDS1 protein, S cerevisiaeProtein Serine-Threonine KinasesRAD53 protein, S cerevisiaeSaccharomyces cerevisiae ProteinsSecurinTEL1 protein, S cerevisiaeChromosome segregationCyclin Dependent Kinase (Cdk1)DNA damage response (DDR)Genomic instabilityS Phase checkpointSpindle assembly checkpoint (SAC)

Identifiers

PMID27488803
PMCPMC5383677
OpenAlexW2502135420

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.