Evidence map›Paper›PMID 33289333›Full record

ArticleEMBO reports2021

Non-recombinogenic roles for Rad52 in translesion synthesis during DNA damage tolerance.

María I Cano-Linares, Aurora Yáñez-Vilches, Néstor García-Rodríguez, Marta Barrientos-Moreno, Román González-Prieto, Pedro San-Segundo, Helle D Ulrich, Félix Prado

Open access · bronzeAbstract read
In one paragraph

Article in EMBO reports, 2021. 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
1.4field-weighted citation impact, top 18% 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, 39 citations in OpenAlex.

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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 3 institutions in 2 countries.

María I Cano-LinaresDepartment of Genome Biology, Andalusian Molecular Biology and Regenerative Medicine Center (CABIMER), CSIC-University of Seville-University Pablo de Olavide, Seville, Spain.
Aurora Yáñez-VilchesDepartment of Genome Biology, Andalusian Molecular Biology and Regenerative Medicine Center (CABIMER), CSIC-University of Seville-University Pablo de Olavide, Seville, Spain.
Néstor García-RodríguezInstitute of Molecular Biology (IMB), Mainz, Germany.
Marta Barrientos-MorenoDepartment of Genome Biology, Andalusian Molecular Biology and Regenerative Medicine Center (CABIMER), CSIC-University of Seville-University Pablo de Olavide, Seville, Spain.
Román González-PrietoDepartment of Genome Biology, Andalusian Molecular Biology and Regenerative Medicine Center (CABIMER), CSIC-University of Seville-University Pablo de Olavide, Seville, Spain.ORCID 0000-0001-8997-2321
Pedro San-SegundoInstitute of Functional Biology and Genomics (IBFG), CSIC-University of Salamanca, Salamanca, Spain.
Helle D UlrichInstitute of Molecular Biology (IMB), Mainz, Germany.ORCID 0000-0003-0431-2223
Félix PradoDepartment of Genome Biology, Andalusian Molecular Biology and Regenerative Medicine Center (CABIMER), CSIC-University of Seville-University Pablo de Olavide, Seville, Spain.ORCID 0000-0001-9805-782X
Centro Andaluz de Biología Molecular y Medicina Regenerativa · ESInstitute of Molecular Biology · DEUniversidad de Salamanca · ES

Funding

European Research Council ERC AdG323179Marie Curie MSCA-IF-2017-794054
6 · The paper itself

Abstract

DNA damage tolerance relies on homologous recombination (HR) and translesion synthesis (TLS) mechanisms to fill in the ssDNA gaps generated during passing of the replication fork over DNA lesions in the template. Whereas TLS requires specialized polymerases able to incorporate a dNTP opposite the lesion and is error-prone, HR uses the sister chromatid and is mostly error-free. We report that the HR protein Rad52-but not Rad51 and Rad57-acts in concert with the TLS machinery (Rad6/Rad18-mediated PCNA ubiquitylation and polymerases Rev1/Pol ζ) to repair MMS and UV light-induced ssDNA gaps through a non-recombinogenic mechanism, as inferred from the different phenotypes displayed in the absence of Rad52 and Rad54 (essential for MMS- and UV-induced HR); accordingly, Rad52 is required for efficient DNA damage-induced mutagenesis. In addition, Rad52, Rad51, and Rad57, but not Rad54, facilitate Rad6/Rad18 binding to chromatin and subsequent DNA damage-induced PCNA ubiquitylation. Therefore, Rad52 facilitates the tolerance process not only by HR but also by TLS through Rad51/Rad57-dependent and -independent processes, providing a novel role for the recombination proteins in maintaining genome integrity.

Indexed as

DNA DamageDNA RepairDNA ReplicationRad52 DNA Repair and Recombination ProteinDNA-Directed DNA PolymeraseDNA, Single-StrandedDNA-Directed DNA PolymeraseDNA, Single-StrandedRad52 DNA Repair and Recombination ProteinDNA damage tolerancehomologous recombinationRad52template switchingtranslesion synthesis

Identifiers

PMID33289333
PMCPMC7788459
OpenAlexW3107670372

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.