Evidence map›Paper›PMID 29946146›Full record

ArticleScientific reports2018

Double Strand Break DNA Repair occurs via Non-Homologous End-Joining in Mouse MII Oocytes.

Jacinta H Martin, Elizabeth G Bromfield, R John Aitken, Tessa Lord, Brett Nixon

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.4field-weighted citation impact, top 8% 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

24 citing papers in PubMed, 40 citations in OpenAlex.

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  15. Frontiers in endocrinology · 2023
    Article
  16. Review
  17. Article
  18. Review
  19. DNA Repair in Haploid Context.International journal of molecular sciences · 2021
    Review
  20. DNA repair in primordial follicle oocytes following cisplatin treatment.Journal of assisted reproduction and genetics · 2021
    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

5 authors at 2 institutions in 2 countries.

Jacinta H MartinPriority Research Centre for Reproductive Science, School of Environmental and Life Sciences, The University of Newcastle, Callaghan, NSW, 2308, Australia. Jacinta.martin@newcastle.edu.au.ORCID 0000-0002-0876-5150
Elizabeth G BromfieldPriority Research Centre for Reproductive Science, School of Environmental and Life Sciences, The University of Newcastle, Callaghan, NSW, 2308, Australia.
R John AitkenPriority Research Centre for Reproductive Science, School of Environmental and Life Sciences, The University of Newcastle, Callaghan, NSW, 2308, Australia.
Tessa LordSchool of Molecular Biosciences, Centre for Reproductive Biology, College of Veterinary Medicine, Washington State University, Pullman, WA, 99164, USA.
Brett NixonPriority Research Centre for Reproductive Science, School of Environmental and Life Sciences, The University of Newcastle, Callaghan, NSW, 2308, Australia.ORCID 0000-0003-2745-8188
Hunter Medical Research Institute · AUWashington State University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The unique biology of the oocyte means that accepted paradigms for DNA repair and protection are not of direct relevance to the female gamete. Instead, preservation of the integrity of the maternal genome depends on endogenous protein stores and/or mRNA transcripts accumulated during oogenesis. The aim of this study was to determine whether mature (MII) oocytes have the capacity to detect DNA damage and subsequently mount effective repair. For this purpose, DNA double strand breaks (DSB) were elicited using the topoisomerase II inhibitor, etoposide (ETP). ETP challenge led to a rapid and significant increase in DSB (P = 0.0002) and the consequential incidence of metaphase plate abnormalities (P = 0.0031). Despite this, ETP-treated MII oocytes retained their ability to participate in in vitro fertilisation, though displayed reduced developmental competence beyond the 2-cell stage (P = 0.02). To account for these findings, we analysed the efficacy of DSB resolution, revealing a significant reduction in DSB lesions 4 h post-ETP treatment. Notably, this response was completely abrogated by pharmacological inhibition of key elements (DNA-PKcs and DNA ligase IV) of the canonical non-homologous end joining DNA repair pathway, thus providing the first evidence implicating this reparative cascade in the protection of the maternal genome.

Indexed as

DNA Breaks, Double-StrandedAnimalsDNA DamageDNA RepairEtoposideMiceOocytesTopoisomerase II InhibitorsEtoposideTopoisomerase II Inhibitors

Identifiers

PMID29946146
PMCPMC6018751
OpenAlexW2809081803

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.