Evidence map›Paper›PMID 37058556›Full record

ArticleScience advances2023

Polymerase iota (Pol ι) prevents PrimPol-mediated nascent DNA synthesis and chromosome instability.

Sabrina F Mansilla, Agostina P Bertolin, Sofía Venerus Arbilla, Bryan A Castaño, Tiya Jahjah, Jenny K Singh, Sebastián O Siri, María Victoria Castro, María Belén de la Vega, Annabel Quinet and 2 more

Open access · goldAbstract read
In one paragraph

Article in Science advances, 2023. 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
2.9field-weighted citation impact, top 9% 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, 19 citations in OpenAlex.

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  11. E3 ubiquitin ligase RNF2 protects polymerase ι from destabilization.Biochimica et biophysica acta. Molecular cell research · 2024
    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 4 institutions in 4 countries.

Sabrina F MansillaFundación Instituto Leloir, CONICET, 1405 Buenos Aires, Argentina.ORCID 0000-0001-7752-3377
Agostina P BertolinFundación Instituto Leloir, CONICET, 1405 Buenos Aires, Argentina.ORCID 0000-0002-4808-8254
Sofía Venerus ArbillaFundación Instituto Leloir, CONICET, 1405 Buenos Aires, Argentina.ORCID 0000-0003-2826-7615
Bryan A CastañoDepartment of Obstetrics and Gynecology, Ulm University, 89075 Ulm, Germany.
Tiya JahjahUniversité Paris Cité, Inserm, CEA, Stabilité Génétique Cellules Souches et Radiations, LRS/iRCM/IBFJ, F-92265 Fontenay-aux-Roses, France.ORCID 0000-0001-8065-7325
Jenny K SinghUniversité Paris Cité, Inserm, CEA, Stabilité Génétique Cellules Souches et Radiations, LRS/iRCM/IBFJ, F-92265 Fontenay-aux-Roses, France.ORCID 0000-0001-7222-7317
Sebastián O SiriFundación Instituto Leloir, CONICET, 1405 Buenos Aires, Argentina.
María Victoria CastroFundación Instituto Leloir, CONICET, 1405 Buenos Aires, Argentina.ORCID 0000-0002-2505-3120
María Belén de la VegaFundación Instituto Leloir, CONICET, 1405 Buenos Aires, Argentina.ORCID 0009-0006-3775-9805
Annabel QuinetUniversité Paris Cité, Inserm, CEA, Stabilité Génétique Cellules Souches et Radiations, LRS/iRCM/IBFJ, F-92265 Fontenay-aux-Roses, France.ORCID 0000-0003-0852-6181
Lisa WiesmüllerDepartment of Obstetrics and Gynecology, Ulm University, 89075 Ulm, Germany.ORCID 0000-0002-2397-5041
Vanesa GottifrediFundación Instituto Leloir, CONICET, 1405 Buenos Aires, Argentina.ORCID 0000-0001-9656-5951
Fundación Instituto Leloir · ARInserm · FRUniversität Ulm · DEThe Francis Crick Institute · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent studies have described a DNA damage tolerance pathway choice that involves a competition between PrimPol-mediated repriming and fork reversal. Screening different translesion DNA synthesis (TLS) polymerases by the use of tools for their depletion, we identified a unique role of Pol ι in regulating such a pathway choice. Pol ι deficiency unleashes PrimPol-dependent repriming, which accelerates DNA replication in a pathway that is epistatic with ZRANB3 knockdown. In Pol ι-depleted cells, the excess participation of PrimPol in nascent DNA elongation reduces replication stress signals, but thereby also checkpoint activation in S phase, triggering chromosome instability in M phase. This TLS-independent function of Pol ι requires its PCNA-interacting but not its polymerase domain. Our findings unravel an unanticipated role of Pol ι in protecting the genome stability of cells from detrimental changes in DNA replication dynamics caused by PrimPol.

Indexed as

DNA-Directed DNA PolymeraseDNA ReplicationChromosomal InstabilityDNADNA DamageDNA PrimaseDNA RepairHumansMultifunctional EnzymesDNADNA-Directed DNA PolymeraseDNA PrimaseMultifunctional EnzymesPrimPol protein, human

Identifiers

PMID37058556
PMCPMC10104471
OpenAlexW4365504627

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.