Evidence map›Paper›PMID 29717169›Full record

ArticleScientific reports2018

UNG-1 and APN-1 are the major enzymes to efficiently repair 5-hydroxymethyluracil DNA lesions in C. elegans.

Arturo Papaluca, J Richard Wagner, H Uri Saragovi, Dindial Ramotar

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 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

12 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. A Brief Review on Caenorhabditis elegans Role in Modelling Neurodegenerative Disease.Central nervous system agents in medicinal chemistry · 2025
    Review
  3. Review
  4. Frontiers in aging · 2022
    Review
  5. Review
  6. Article
  7. Review
  8. The Base Excision Repair Pathway in the NematodeFrontiers in cell and developmental biology · 2020
    Review
  9. Article
  10. Article
  11. Article
  12. Sequencing 5-Hydroxymethyluracil at Single-Base Resolution.Angewandte Chemie (International ed. in English) · 2018
    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

4 authors at 3 institutions in 1 country.

Arturo PapalucaMaisonneuve-Rosemont Hospital, Research Center, Université de Montréal, Department of Medicine, 5415 Boul. de l'Assomption, Montréal, Québec, H1T2M4, Canada.
J Richard WagnerDépartement de Médecine Nucléaire et Radiobiologie, Faculté de Médecine et des Sciences de la Santé, Université de Sherbrooke, 3001 12 Avenue Nord, Sherbrooke, Québec, J1H5N4, Canada.
H Uri SaragoviLady Davis Institute for Medical Research, Jewish General Hospital, McGill University, Department of Pharmacology and Therapeutics, McGill University, Department of Pharmacology and Therapeutics, 3755 Chemin de la Côte Sainte-Catherine, Québec, Montréal, H3T1E2, Canada.
Dindial RamotarMaisonneuve-Rosemont Hospital, Research Center, Université de Montréal, Department of Medicine, 5415 Boul. de l'Assomption, Montréal, Québec, H1T2M4, Canada. dindial.ramotar@umontreal.ca.ORCID 0000-0002-9572-7223
Jewish General Hospital · CAHôpital Maisonneuve-Rosemont · CAUniversité de Sherbrooke · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In Caenorhabditis elegans, two DNA glycosylases, UNG-1 and NTH-1, and two AP endonucleases, APN-1 and EXO-3, have been characterized from the base-excision repair (BER) pathway that repairs oxidatively modified DNA bases. UNG-1 removes uracil, while NTH-1 can remove 5-hydroxymethyluracil (5-hmU), an oxidation product of thymine, as well as other lesions. Both APN-1 and EXO-3 can incise AP sites and remove 3'-blocking lesions at DNA single strand breaks, and only APN-1 possesses 3'- to 5'-exonulease and nucleotide incision repair activities. We used C. elegans mutants to study the role of the BER pathway in processing 5-hmU. We observe that ung-1 mutants exhibited a decrease in brood size and lifespan, and an elevated level of germ cell apoptosis when challenged with 5-hmU. These phenotypes were exacerbated by RNAi downregulation of apn-1 in the ung-1 mutant. The nth-1 or exo-3 mutants displayed wild type phenotypes towards 5-hmU. We show that partially purified UNG-1 can act on 5-hmU lesion in vitro. We propose that UNG-1 removes 5-hmU incorporated into the genome and the resulting AP site is cleaved by APN-1 or EXO-3. In the absence of UNG-1, the 5-hmU is removed by NTH-1 creating a genotoxic 3'-blocking lesion that requires the action of APN-1.

Indexed as

Caenorhabditis elegansAnimalsApoptosisCaenorhabditis elegans ProteinsDNA-(Apurinic or Apyrimidinic Site) LyaseDNA DamageDNA GlycosylasesDNA RepairEndodeoxyribonucleasesEndonucleasesGerm CellsLongevityLoss of Function MutationPentoxylUracil-DNA Glycosidase5-hydroxymethyluracilapn-1 protein, C elegansCaenorhabditis elegans ProteinsDNA-(Apurinic or Apyrimidinic Site) LyaseDNA GlycosylasesEndodeoxyribonucleasesEndonucleasesEXO-3 protein, C elegansNTH-1 protein, C elegansPentoxylung-1 protein, C elegansUracil-DNA Glycosidase

Identifiers

PMID29717169
PMCPMC5931555
OpenAlexW2806981460

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.