Evidence map›Paper›PMID 27672038›Full record

ArticleNucleic acids research2016

Nucleolytic processing of aberrant replication intermediates by an Exo1-Dna2-Sae2 axis counteracts fork collapse-driven chromosome instability.

Arianna Colosio, Camilla Frattini, Grazia Pellicanò, Sara Villa-Hernández, Rodrigo Bermejo

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

19 citing papers in PubMed, 24 citations in OpenAlex.

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  11. EssentialProceedings of the National Academy of Sciences of the United States of America · 2019
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  13. CaMolecular cell · 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

5 authors at 3 institutions in 2 countries.

Arianna ColosioThe F.I.R.C. Institute of Molecular Oncology (IFOM) Foundation, Via Adamello 16, 20139 Milan, Italy.
Camilla FrattiniInstituto de Biología Funcional y Genómica (IBFG-CSIC), Universidad de Salamanca, Calle Zacarías González 2, 37007 Salamanca, Spain.
Grazia PellicanòCentro de Investigaciones Biológicas (CIB-CSIC), Calle Ramiro de Maeztu 9, 28040 Madrid, Spain.
Sara Villa-HernándezInstituto de Biología Funcional y Genómica (IBFG-CSIC), Universidad de Salamanca, Calle Zacarías González 2, 37007 Salamanca, Spain.
Rodrigo BermejoInstituto de Biología Funcional y Genómica (IBFG-CSIC), Universidad de Salamanca, Calle Zacarías González 2, 37007 Salamanca, Spain rodrigo.bermejo@csic.es.ORCID 0000-0002-2692-7045
Universidad de Salamanca · ESCentro de Investigaciones Biológicas Margarita Salas · ESIFOM · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Problems during DNA replication underlie genomic instability and drive malignant transformation. The DNA damage checkpoint stabilizes stalled replication forks thus counteracting aberrant fork transitions, DNA breaks and chromosomal rearrangements. We analyzed fork processing in checkpoint deficient cells by coupling psoralen crosslinking with replication intermediate two-dimensional gel analysis. This revealed a novel role for Exo1 nuclease in resecting reversed replication fork structures and counteracting the accumulation of aberrant intermediates resembling fork cleavage products. Genetic analyses demonstrated a functional interplay of Exo1 with Mus81, Dna2 and Sae2 nucleases in promoting cell survival following replication stress, suggestive of concerted nucleolytic processing of stalled forks. While Mus81 and other Structure Specific Endonucleases do not contribute to obvious collapsed fork transitions, Dna2 promotes reversed fork resection likely by facilitating Exo1 access to nascent strands. Instead, Sae2 cooperates with Exo1 in counteracting putative fork cleavage events linked to double strand breaks formation and increased gross chromosomal rearrangement rates. Our data indicate that in checkpoint deficient cells diverse nuclease activities interface to eliminate aberrant replication intermediates and prevent chromosome instability.

Indexed as

DNA ReplicationCell Cycle ProteinsCheckpoint Kinase 2Chromosomal InstabilityChromosomes, FungalDNA, FungalDNA HelicasesDNA RepairEndonucleasesExodeoxyribonucleasesG1 Phase Cell Cycle CheckpointsSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsCell Cycle ProteinsCheckpoint Kinase 2DNA2 protein, S cerevisiaeDNA, FungalDNA HelicasesEndonucleasesexodeoxyribonuclease IExodeoxyribonucleasesRAD53 protein, S cerevisiaeSaccharomyces cerevisiae ProteinsSAE2 protein, S cerevisiae

Identifiers

PMID27672038
PMCPMC5159547
OpenAlexW2526186974

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.