Evidence map›Paper›PMID 27852625›Full record

ArticleThe EMBO journal2017

Stabilization of the metaphase spindle by Cdc14 is required for recombinational DNA repair.

María Teresa Villoria, Facundo Ramos, Encarnación Dueñas, Peter Faull, Pedro Rodríguez Cutillas, Andrés Clemente-Blanco

Open access · bronzeAbstract read
In one paragraph

Article in The EMBO journal, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

21 citing papers in PubMed, 32 citations in OpenAlex.

  1. Yeast centrosomes act as organizing centers to promote Polo kinase-mediated adaptation to persistent DNA damage.Proceedings of the National Academy of Sciences of the United States of America · 2025
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  12. The Multiple Roles of the Cdc14 Phosphatase in Cell Cycle Control.International journal of molecular sciences · 2020
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  18. Lsm12 Mediates Deubiquitination of DNA Polymerase η To HelpApplied and environmental microbiology · 2019
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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 at 2 institutions in 2 countries.

María Teresa VilloriaCell Cycle and Genome Stability Group, Instituto de Biología Funcional y Genómica Consejo Superior de Investigaciones Científicas (CSIC) Universidad de Salamanca (USAL), Salamanca, Spain.
Facundo RamosCell Cycle and Genome Stability Group, Instituto de Biología Funcional y Genómica Consejo Superior de Investigaciones Científicas (CSIC) Universidad de Salamanca (USAL), Salamanca, Spain.
Encarnación DueñasCell Cycle and Genome Stability Group, Instituto de Biología Funcional y Genómica Consejo Superior de Investigaciones Científicas (CSIC) Universidad de Salamanca (USAL), Salamanca, Spain.
Peter FaullBiological Mass Spectrometry and Proteomics Laboratory, Medical Research Council Clinical Science Centre Imperial College, London, UK.
Pedro Rodríguez CutillasBiological Mass Spectrometry and Proteomics Laboratory, Medical Research Council Clinical Science Centre Imperial College, London, UK.
Andrés Clemente-BlancoCell Cycle and Genome Stability Group, Instituto de Biología Funcional y Genómica Consejo Superior de Investigaciones Científicas (CSIC) Universidad de Salamanca (USAL), Salamanca, Spain andresclemente@usal.es.ORCID 0000-0002-3674-0671
Consejo Superior de Investigaciones Científicas · ESImperial College London · GB

Funding

Biotechnology and Biological Sciences Research Council BB/M006174/1
6 · The paper itself

Abstract

Cells are constantly threatened by multiple sources of genotoxic stress that cause DNA damage. To maintain genome integrity, cells have developed a coordinated signalling network called DNA damage response (DDR). While multiple kinases have been thoroughly studied during DDR activation, the role of protein dephosphorylation in the damage response remains elusive. Here, we show that the phosphatase Cdc14 is essential to fulfil recombinational DNA repair in budding yeast. After DNA double-strand break (DSB) generation, Cdc14 is transiently released from the nucleolus and activated. In this state, Cdc14 targets the spindle pole body (SPB) component Spc110 to counterbalance its phosphorylation by cyclin-dependent kinase (Cdk). Alterations in the Cdk/Cdc14-dependent phosphorylation status of Spc110, or its inactivation during the induction of a DNA lesion, generate abnormal oscillatory SPB movements that disrupt DSB-SPB interactions. Remarkably, these defects impair DNA repair by homologous recombination indicating that SPB integrity is essential during the repair process. Together, these results show that Cdc14 promotes spindle stability and DSB-SPB tethering during DNA repair, and imply that metaphase spindle maintenance is a critical feature of the repair process.

Indexed as

MetaphaseRecombinational DNA RepairCalmodulin-Binding ProteinsCell Cycle ProteinsCyclin-Dependent KinasesCytoskeletal ProteinsDNA Breaks, Double-StrandedNuclear ProteinsProtein Tyrosine PhosphatasesSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsSpindle ApparatusCalmodulin-Binding ProteinsCDC14 protein, S cerevisiaeCell Cycle ProteinsCyclin-Dependent KinasesCytoskeletal ProteinsNuclear ProteinsProtein Tyrosine PhosphatasesSaccharomyces cerevisiae ProteinsSPC110 protein, S cerevisiaeCdc14DNA repairdouble‐strand breakhomologous recombinationspindle pole body

Identifiers

PMID27852625
PMCPMC5210157
OpenAlexW2551245297

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.