Evidence map›Paper›PMID 18634905›Full record

ArticleDNA repair2008

Reduced efficiency and increased mutagenicity of translesion DNA synthesis across a TT cyclobutane pyrimidine dimer, but not a TT 6-4 photoproduct, in human cells lacking DNA polymerase eta.

Ayal Hendel, Omer Ziv, Quentin Gueranger, Nicholas Geacintov, Zvi Livneh

Open access · greenAbstract read
In one paragraph

Article in DNA repair, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing 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

30 citing papers in PubMed, 57 citations in OpenAlex.

  1. Article
  2. 8-Oxoadenine: A «New» Player of the Oxidative Stress in Mammals?International journal of molecular sciences · 2024
    Review
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. The roles of polymerases ν and θ in replicative bypass ofThe Journal of biological chemistry · 2020
    Article
  9. Review
  10. Repair and translesion synthesis ofThe Journal of biological chemistry · 2019
    Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Genomic assay reveals tolerance of DNA damage by both translesion DNA synthesis and homology-dependent repair in mammalian cells.Proceedings of the National Academy of Sciences of the United States of America · 2013
    Article
  19. Article
  20. Translesion DNA synthesis and mutagenesis in eukaryotes.Cold Spring Harbor perspectives in biology · 2013
    Review
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

5 authors at 3 institutions in 3 countries.

Ayal HendelDepartment of Biological Chemistry, Weizmann Institute of Science, Rehovot 76100, Israel.
Omer Ziv
Quentin Gueranger
Nicholas Geacintov
Zvi Livneh
Weizmann Institute of Science · ILDélégation Paris 5 · FRNew York University · US

Funding

Impact of PAH-DNA Lesions on DNA Repair and ReplicationR01CA099194 · NCI · NEW YORK UNIVERSITY · PI GEACINTOV, NICHOLAS E · 2003 to 2012
$3.3M
NCI NIH HHS CA 099194NCI NIH HHS R01 CA099194
6 · The paper itself

Abstract

Xeroderma pigmentosum variant (XPV) patients carry germ-line mutations in DNA polymerase eta (poleta), a major translesion DNA synthesis (TLS) polymerase, and exhibit severe sunlight sensitivity and high predisposition to skin cancer. Using a quantitative TLS assay system based on gapped plasmids we analyzed TLS across a site-specific TT CPD (thymine-thymine cyclobutane pyrimidine dimer) or TT 6-4 PP (thymine-thymine 6-4 photoproduct) in three pairs of poleta-proficient and deficient human cells. TLS across the TT CPD lesion was reduced by 2.6-4.4-fold in cells lacking poleta, and exhibited a strong 6-17-fold increase in mutation frequency at the TT CPD. All targeted mutations (74%) in poleta-deficient cells were opposite the 3'T of the CPD, however, a significant fraction (23%) were semi-targeted to the nearest nucleotides flanking the CPD. Deletions and insertions were observed at a low frequency, which increased in the absence of poleta, consistent with the formation of double strand breaks due to defective TLS. TLS across TT 6-4 PP was about twofold lower than across CPD, and was marginally reduced in poleta-deficient cells. TLS across TT 6-4 PP was highly mutagenic (27-63%), with multiple mutations types, and no significant difference between cells with or without poleta. Approximately 50% of the mutations formed were semi-targeted, of which 84-93% were due to the insertion of an A opposite the template G 5' to the 6-4 PP. These results, which are consistent with the UV hyper-mutability of XPV cells, highlight the critical role of poleta in error-free TLS across CPD in human cells, and suggest a potential involvement, although minor, of poleta in TLS across 6-4 PP under some conditions.

Indexed as

MutagenesisCells, CulturedDNADNA-Directed DNA PolymeraseFibroblastsHumansPlasmidsPyrimidine DimersSequence Analysis, DNAXeroderma PigmentosumY-Family DNA PolymerasesDNADNA-Directed DNA PolymerasePyrimidine DimersRad30 proteinY-Family DNA Polymerases

Identifiers

PMID18634905
PMCPMC2656611
OpenAlexW2056595058

What OpenQuestion holds

Textmetadata
LicenceTDM
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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.