Evidence map›Paper›PMID 37791890›Full record

ArticleNucleic acids research2023

DNA mismatch repair protects the genome from oxygen-induced replicative mutagenesis.

Rita Lózsa, Eszter Németh, Judit Z Gervai, Bence G Márkus, Sándor Kollarics, Zsolt Gyüre, Judit Tóth, Ferenc Simon, Dávid Szüts

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
3.3field-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

9 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. DNA Damage and Repair in Pancreatic Cancer-The Latest Findings.International journal of molecular sciences · 2025
    Review
  7. Article
  8. Article
  9. 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

9 authors at 4 institutions in 2 countries.

Rita LózsaInstitute of Enzymology, Research Centre for Natural Sciences, H-1117 Budapest, Hungary.
Eszter NémethInstitute of Enzymology, Research Centre for Natural Sciences, H-1117 Budapest, Hungary.
Judit Z GervaiInstitute of Enzymology, Research Centre for Natural Sciences, H-1117 Budapest, Hungary.
Bence G MárkusStavropoulos Center for Complex Quantum Matter, Department of Physics and Astronomy, University of Notre Dame, Notre Dame, IN 46556, USA.ORCID 0000-0003-1472-0482
Sándor KollaricsInstitute for Solid State Physics and Optics, Wigner Research Centre for Physics, H-1525 Budapest, Hungary.
Zsolt GyüreInstitute of Enzymology, Research Centre for Natural Sciences, H-1117 Budapest, Hungary.
Judit TóthInstitute of Enzymology, Research Centre for Natural Sciences, H-1117 Budapest, Hungary.ORCID 0000-0002-0965-046X
Ferenc SimonInstitute for Solid State Physics and Optics, Wigner Research Centre for Physics, H-1525 Budapest, Hungary.
Dávid SzütsInstitute of Enzymology, Research Centre for Natural Sciences, H-1117 Budapest, Hungary.ORCID 0000-0001-7985-0136
Institute of Molecular Life Sciences · HUBudapest University of Technology and Economics · HUSemmelweis University · HUUniversity of Notre Dame · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

DNA mismatch repair (MMR) corrects mismatched DNA bases arising from multiple sources including polymerase errors and base damage. By detecting spontaneous mutagenesis using whole genome sequencing of cultured MMR deficient human cell lines, we show that a primary role of MMR is the repair of oxygen-induced mismatches. We found an approximately twofold higher mutation rate in MSH6 deficient DLD-1 cells or MHL1 deficient HCT116 cells exposed to atmospheric conditions as opposed to mild hypoxia, which correlated with oxidant levels measured using electron paramagnetic resonance spectroscopy. The oxygen-induced mutations were dominated by T to C base substitutions and single T deletions found primarily on the lagging strand. A broad sequence context preference, dependence on replication timing and a lack of transcriptional strand bias further suggested that oxygen-induced mutations arise from polymerase errors rather than oxidative base damage. We defined separate low and high oxygen-specific MMR deficiency mutation signatures common to the two cell lines and showed that the effect of oxygen is observable in MMR deficient cancer genomes, where it best correlates with the contribution of mutation signature SBS21. Our results imply that MMR corrects oxygen-induced genomic mismatches introduced by a replicative process in proliferating cells.

Indexed as

DNA Mismatch RepairMutagenesisOxygenBase Pair MismatchCell LineDNA RepairDNA ReplicationHumansMutationOxygen

Identifiers

PMID37791890
PMCPMC10639081
OpenAlexW4387327038

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.