Evidence map›Paper›PMID 30158111›Full record

ArticleThe EMBO journal2018

Mrc1 and Rad9 cooperate to regulate initiation and elongation of DNA replication in response to DNA damage.

Julien Bacal, María Moriel-Carretero, Benjamin Pardo, Antoine Barthe, Sushma Sharma, Andrei Chabes, Armelle Lengronne, Philippe Pasero

Open access · bronzeAbstract read
In one paragraph

Article in The EMBO journal, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

43 citing papers in PubMed, 67 citations in OpenAlex.

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  17. Rad53 arrests leading and lagging strand DNA synthesis via distinct mechanisms in response to DNA replication stress.BioEssays : news and reviews in molecular, cellular and developmental biology · 2022
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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

8 authors at 2 institutions in 2 countries.

Julien BacalInstitut de Génétique Humaine, CNRS, Equipe Labellisée Ligue contre le Cancer, Université de Montpellier, Montpellier, France.
María Moriel-CarreteroInstitut de Génétique Humaine, CNRS, Equipe Labellisée Ligue contre le Cancer, Université de Montpellier, Montpellier, France.
Benjamin PardoInstitut de Génétique Humaine, CNRS, Equipe Labellisée Ligue contre le Cancer, Université de Montpellier, Montpellier, France.
Antoine BartheInstitut de Génétique Humaine, CNRS, Equipe Labellisée Ligue contre le Cancer, Université de Montpellier, Montpellier, France.
Sushma SharmaDepartment of Medical Biochemistry and Biophysics and Laboratory for Molecular Infection Medicine Sweden (MIMS), Umeå University, Umeå, Sweden.
Andrei ChabesDepartment of Medical Biochemistry and Biophysics and Laboratory for Molecular Infection Medicine Sweden (MIMS), Umeå University, Umeå, Sweden.ORCID 0000-0003-1708-8259
Armelle LengronneInstitut de Génétique Humaine, CNRS, Equipe Labellisée Ligue contre le Cancer, Université de Montpellier, Montpellier, France.
Philippe PaseroInstitut de Génétique Humaine, CNRS, Equipe Labellisée Ligue contre le Cancer, Université de Montpellier, Montpellier, France ppasero@igh.cnrs.fr.ORCID 0000-0001-5891-0822
Centre National de la Recherche Scientifique · FRUmeå University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The S-phase checkpoint maintains the integrity of the genome in response to DNA replication stress. In budding yeast, this pathway is initiated by Mec1 and is amplified through the activation of Rad53 by two checkpoint mediators: Mrc1 promotes Rad53 activation at stalled forks, and Rad9 is a general mediator of the DNA damage response. Here, we have investigated the interplay between Mrc1 and Rad9 in response to DNA damage and found that they control DNA replication through two distinct but complementary mechanisms. Mrc1 rapidly activates Rad53 at stalled forks and represses late-firing origins but is unable to maintain this repression over time. Rad9 takes over Mrc1 to maintain a continuous checkpoint signaling. Importantly, the Rad9-mediated activation of Rad53 slows down fork progression, supporting the view that the S-phase checkpoint controls both the initiation and the elongation of DNA replication in response to DNA damage. Together, these data indicate that Mrc1 and Rad9 play distinct functions that are important to ensure an optimal completion of S phase under replication stress conditions.

Indexed as

DNA DamageDNA ReplicationCell Cycle ProteinsCheckpoint Kinase 2DNA, FungalSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsS PhaseCell Cycle ProteinsCheckpoint Kinase 2DNA, FungalMRC1 protein, S cerevisiaeRAD53 protein, S cerevisiaerad9 proteinSaccharomyces cerevisiae ProteinsDNA replicationelongationinitiationS‐phase checkpoint

Identifiers

PMID30158111
PMCPMC6213276
OpenAlexW2889044344

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.