Evidence map›Paper›PMID 27095204›Full record

ArticleNucleic acids research2016

Translesion synthesis mechanisms depend on the nature of DNA damage in UV-irradiated human cells.

Annabel Quinet, Davi Jardim Martins, Alexandre Teixeira Vessoni, Denis Biard, Alain Sarasin, Anne Stary, Carlos Frederico Martins Menck

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 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
3.8field-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

50 citing papers in PubMed, 78 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

7 authors at 5 institutions in 3 countries.

Annabel QuinetInstitute of Biomedical Sciences, University of São Paulo, SP, 05508-000, Brazil annabel.quinet@gmail.com.
Davi Jardim MartinsInstitute of Biomedical Sciences, University of São Paulo, SP, 05508-000, Brazil.
Alexandre Teixeira VessoniInstitute of Biomedical Sciences, University of São Paulo, SP, 05508-000, Brazil.
Denis BiardCEA, IMETI, SEPIA, Team Cellular Engineering and Human Syndromes, F-92265 Fontenay-aux-Roses, France.
Alain SarasinCNRS-UMR8200, Université Paris Sud, Institut de Cancérologie Gustave Roussy, 94805 Villejuif, France.
Anne StaryCNRS-UMR8200, Université Paris Sud, Institut de Cancérologie Gustave Roussy, 94805 Villejuif, France.
Carlos Frederico Martins MenckInstitute of Biomedical Sciences, University of São Paulo, SP, 05508-000, Brazil cfmmenck@usp.br.
Hospital Universitário da Universidade de São Paulo · BRBiotherapy of Genetic Diseases, Inflammatory Disorders and Cancers · FRCentre National de la Recherche Scientifique · FRInstitut de Radiobiologie Cellulaire et Moléculaire · FRInstitute of Biomedical Science · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ultraviolet-induced 6-4 photoproducts (6-4PP) and cyclobutane pyrimidine dimers (CPD) can be tolerated by translesion DNA polymerases (TLS Pols) at stalled replication forks or by gap-filling. Here, we investigated the involvement of Polη, Rev1 and Rev3L (Polζ catalytic subunit) in the specific bypass of 6-4PP and CPD in repair-deficient XP-C human cells. We combined DNA fiber assay and novel methodologies for detection and quantification of single-stranded DNA (ssDNA) gaps on ongoing replication forks and postreplication repair (PRR) tracts in the human genome. We demonstrated that Rev3L, but not Rev1, is required for postreplicative gap-filling, while Polη and Rev1 are responsible for TLS at stalled replication forks. Moreover, specific photolyases were employed to show that in XP-C cells, CPD arrest replication forks, while 6-4PP are responsible for the generation of ssDNA gaps and PRR tracts. On the other hand, in the absence of Polη or Rev1, both types of lesion block replication forks progression. Altogether, the data directly show that, in the human genome, Polη and Rev1 bypass CPD and 6-4PP at replication forks, while only 6-4PP are also tolerated by a Polζ-dependent gap-filling mechanism, independent of S phase.

Indexed as

DNA RepairDNA ReplicationAdenoviridaeCell Line, TransformedDeoxyribodipyrimidine Photo-LyaseDNA-Binding ProteinsDNA DamageDNA-Directed DNA PolymeraseDNA, Single-StrandedFibroblastsGenetic VectorsGenome, HumanHumansNuclear ProteinsNucleotidyltransferasesPyrimidine DimersDeoxyribodipyrimidine Photo-LyaseDNA-Binding ProteinsDNA-Directed DNA PolymeraseDNA, Single-StrandedNuclear ProteinsNucleotidyltransferasesPyrimidine Dimerspyrimidine-pyrimidone dimerRad30 proteinREV1 protein, humanREV3L protein, humanY-Family DNA Polymerases

Identifiers

PMID27095204
PMCPMC4937316
OpenAlexW2340964324

What OpenQuestion holds

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LicenceCC BY-NC
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.