Evidence map›Paper›PMID 29165708›Full record

ArticleNucleic acids research2018

Separase prevents genomic instability by controlling replication fork speed.

Francesco Cucco, Elisa Palumbo, Serena Camerini, Barbara D'Alessio, Valentina Quarantotti, Maria Luisa Casella, Ilaria Maria Rizzo, Dubravka Cukrov, Domenico Delia, Antonella Russo and 2 more

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

16 citing papers in PubMed, 23 citations in OpenAlex.

  1. Trial
  2. Article
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  5. Article
  6. The multifaceted roles of cohesin in cancer.Journal of experimental & clinical cancer research : CR · 2022
    Review
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  8. Review
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  11. Review
  12. Overexpression of the cohesin-core subunit SMC1A contributes to colorectal cancer development.Journal of experimental & clinical cancer research : CR · 2019
    Article
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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

12 authors at 6 institutions in 1 country.

Francesco CuccoInstitute for Biomedical and Genetic Research, National Research Council, Pisa, Italy.
Elisa PalumboDepartment of Biology, University of Padua, Padua, Italy.
Serena CameriniDepartment of Cell Biology and Neurosciences, National Institute of Health, Rome, Italy.
Barbara D'AlessioInstitute for Biomedical and Genetic Research, National Research Council, Pisa, Italy.
Valentina QuarantottiInstitute for Biomedical and Genetic Research, National Research Council, Pisa, Italy.
Maria Luisa CasellaDepartment of Cell Biology and Neurosciences, National Institute of Health, Rome, Italy.
Ilaria Maria RizzoInstitute for Biomedical and Genetic Research, National Research Council, Pisa, Italy.
Dubravka CukrovInstitute for Biomedical and Genetic Research, National Research Council, Pisa, Italy.
Domenico DeliaFondazione IRCCS Istituto Nazionale Tumori, Department of Experimental Oncology, Milan, Italy.
Antonella RussoDepartment of Biology, University of Padua, Padua, Italy.
Marco CrescenziDepartment of Cell Biology and Neurosciences, National Institute of Health, Rome, Italy.
Antonio MusioInstitute for Biomedical and Genetic Research, National Research Council, Pisa, Italy.
Istituto Superiore di Sanità · ITNational Research Council · ITInstitute of Genetic and Biomedical Research · ITUniversity of Padua · ITFondazione IRCCS Istituto Nazionale dei Tumori · ITTumour Institute of Tuscany · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Proper chromosome segregation is crucial for preserving genomic integrity, and errors in this process cause chromosome mis-segregation, which may contribute to cancer development. Sister chromatid separation is triggered by Separase, an evolutionary conserved protease that cleaves the cohesin complex, allowing the dissolution of sister chromatid cohesion. Here we provide evidence that Separase participates in genomic stability maintenance by controlling replication fork speed. We found that Separase interacted with the replication licensing factors MCM2-7, and genome-wide data showed that Separase co-localized with MCM complex and cohesin. Unexpectedly, the depletion of Separase increased the fork velocity about 1.5-fold and caused a strong acetylation of cohesin's SMC3 subunit and altered checkpoint response. Notably, Separase silencing triggered genomic instability in both HeLa and human primary fibroblast cells. Our results show a novel mechanism for fork progression mediated by Separase and thus the basis for genomic instability associated with tumorigenesis.

Indexed as

DNA ReplicationGenomic InstabilityNucleic Acid ConformationCell Cycle ProteinsCells, CulturedChromatidsChromosomal Proteins, Non-HistoneChromosome SegregationCohesinsDNAHeLa CellsHumansMinichromosome Maintenance ProteinsModels, GeneticProtein BindingRNA InterferenceCell Cycle ProteinsChromosomal Proteins, Non-HistoneCohesinsDNAMinichromosome Maintenance ProteinsSeparase

Identifiers

PMID29165708
PMCPMC5758895
OpenAlexW2769586039

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.