Evidence map›Paper›PMID 38776358›Full record

ArticlePLoS genetics2024

Physical interactions between specifically regulated subpopulations of the MCM and RNR complexes prevent genetic instability.

Aurora Yáñez-Vilches, Antonia M Romero, Marta Barrientos-Moreno, Esther Cruz, Román González-Prieto, Sushma Sharma, Alfred C O Vertegaal, Félix Prado

Abstract read
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In one paragraph

Article in PLoS genetics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Article
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.

Aurora Yáñez-VilchesCentro Andaluz de Biología Molecular y Medicina Regenerativa-CABIMER, Consejo Superior de Investigaciones Científicas, Universidad de Sevilla, Universidad Pablo de Olavide, Seville, Spain.ORCID 0000-0003-3278-8560
Antonia M RomeroCentro Andaluz de Biología Molecular y Medicina Regenerativa-CABIMER, Consejo Superior de Investigaciones Científicas, Universidad de Sevilla, Universidad Pablo de Olavide, Seville, Spain.ORCID 0000-0002-2727-279X
Marta Barrientos-MorenoCentro Andaluz de Biología Molecular y Medicina Regenerativa-CABIMER, Consejo Superior de Investigaciones Científicas, Universidad de Sevilla, Universidad Pablo de Olavide, Seville, Spain.ORCID 0000-0002-2709-8437
Esther CruzCentro Andaluz de Biología Molecular y Medicina Regenerativa-CABIMER, Consejo Superior de Investigaciones Científicas, Universidad de Sevilla, Universidad Pablo de Olavide, Seville, Spain.
Román González-PrietoCentro Andaluz de Biología Molecular y Medicina Regenerativa-CABIMER, Consejo Superior de Investigaciones Científicas, Universidad de Sevilla, Universidad Pablo de Olavide, Seville, Spain.
Sushma SharmaDepartment of Medical Biochemistry and Biophysics, Umeå University, Umeå, Sweden.ORCID 0000-0003-2713-5813
Alfred C O VertegaalDepartment of Cell and Chemical Biology, Leiden University Medical Center, Leiden, the Netherlands.
Félix PradoCentro Andaluz de Biología Molecular y Medicina Regenerativa-CABIMER, Consejo Superior de Investigaciones Científicas, Universidad de Sevilla, Universidad Pablo de Olavide, Seville, Spain.ORCID 0000-0001-9805-782X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The helicase MCM and the ribonucleotide reductase RNR are the complexes that provide the substrates (ssDNA templates and dNTPs, respectively) for DNA replication. Here, we demonstrate that MCM interacts physically with RNR and some of its regulators, including the kinase Dun1. These physical interactions encompass small subpopulations of MCM and RNR, are independent of the major subcellular locations of these two complexes, augment in response to DNA damage and, in the case of the Rnr2 and Rnr4 subunits of RNR, depend on Dun1. Partial disruption of the MCM/RNR interactions impairs the release of Rad52 -but not RPA-from the DNA repair centers despite the lesions are repaired, a phenotype that is associated with hypermutagenesis but not with alterations in the levels of dNTPs. These results suggest that a specifically regulated pool of MCM and RNR complexes plays non-canonical roles in genetic stability preventing persistent Rad52 centers and hypermutagenesis.

Indexed as

Cell Cycle ProteinsDNA DamageDNA RepairDNA ReplicationGenomic InstabilityRad52 DNA Repair and Recombination ProteinRibonucleotide ReductasesSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsDNA HelicasesMinichromosome Maintenance ProteinsProtein Serine-Threonine KinasesReplication Protein ARibonucleoside Diphosphate ReductaseCell Cycle ProteinsDNA HelicasesDUN1 protein, S cerevisiaeMinichromosome Maintenance ProteinsProtein Serine-Threonine KinasesRad52 DNA Repair and Recombination ProteinRAD52 protein, S cerevisiaeReplication Protein ARibonucleoside Diphosphate ReductaseRibonucleotide ReductasesRNR2 protein, S cerevisiaeSaccharomyces cerevisiae Proteins

Identifiers

PMID38776358
PMCPMC11149843

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Registered trials

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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.