Evidence map›Paper›PMID 24732879›Full record

ArticleScientific reports2014

8-oxoguanine causes spontaneous de novo germline mutations in mice.

Mizuki Ohno, Kunihiko Sakumi, Ryutaro Fukumura, Masato Furuichi, Yuki Iwasaki, Masaaki Hokama, Toshimichi Ikemura, Teruhisa Tsuzuki, Yoichi Gondo, Yusaku Nakabeppu

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers.

0numbers the graph read from it
0cells of the map it votes in
89citing papers in PubMed
6.4field-weighted citation impact, top 3% 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

89 citing papers in PubMed, 185 citations in OpenAlex.

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29 more citing papers are in PubMed but not listed here.

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

10 authors at 3 institutions in 1 country.

Mizuki OhnoDepartment of Medical Biophysics and Radiation Biology, Faculty of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan.
Kunihiko Sakumi1] Division of Neurofunctional Genomics, Department of Immunobiology and Neuroscience, Medical Institute of Bioregulation, Kyushu University, Fukuoka 812-8582, Japan [2] Research Center for Nucleotide Pool, Kyushu University, Fukuoka 812-8582, Japan.
Ryutaro FukumuraMutagenesis and Genomics Team, RIKEN BioResource Center, Tsukuba 305-0074, Japan.
Masato FuruichiRadioisotope Center, Kyushu University, Fukuoka 812-8582, Japan.
Yuki Iwasaki1] Department of Computer Bioscience, Nagahama Institute of Bio-Science and Technology, Nagahama 526-0829, Japan [2] Research Fellow of the Japan Society for the Promotion of Science.
Masaaki HokamaDivision of Neurofunctional Genomics, Department of Immunobiology and Neuroscience, Medical Institute of Bioregulation, Kyushu University, Fukuoka 812-8582, Japan.
Toshimichi IkemuraDepartment of Computer Bioscience, Nagahama Institute of Bio-Science and Technology, Nagahama 526-0829, Japan.
Teruhisa TsuzukiDepartment of Medical Biophysics and Radiation Biology, Faculty of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan.
Yoichi GondoMutagenesis and Genomics Team, RIKEN BioResource Center, Tsukuba 305-0074, Japan.
Yusaku Nakabeppu1] Division of Neurofunctional Genomics, Department of Immunobiology and Neuroscience, Medical Institute of Bioregulation, Kyushu University, Fukuoka 812-8582, Japan [2] Research Center for Nucleotide Pool, Kyushu University, Fukuoka 812-8582, Japan.
Kyushu University · JPNagahama Institute of Bio-Science and Technology · JPRIKEN BioResource Research Center · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Spontaneous germline mutations generate genetic diversity in populations of sexually reproductive organisms, and are thus regarded as a driving force of evolution. However, the cause and mechanism remain unclear. 8-oxoguanine (8-oxoG) is a candidate molecule that causes germline mutations, because it makes DNA more prone to mutation and is constantly generated by reactive oxygen species in vivo. We show here that endogenous 8-oxoG caused de novo spontaneous and heritable G to T mutations in mice, which occurred at different stages in the germ cell lineage and were distributed throughout the chromosomes. Using exome analyses covering 40.9 Mb of mouse transcribed regions, we found increased frequencies of G to T mutations at a rate of 2 × 10(-7) mutations/base/generation in offspring of Mth1/Ogg1/Mutyh triple knockout (TOY-KO) mice, which accumulate 8-oxoG in the nuclear DNA of gonadal cells. The roles of MTH1, OGG1, and MUTYH are specific for the prevention of 8-oxoG-induced mutation, and 99% of the mutations observed in TOY-KO mice were G to T transversions caused by 8-oxoG; therefore, we concluded that 8-oxoG is a causative molecule for spontaneous and inheritable mutations of the germ lineage cells.

Indexed as

AnimalsBase SequenceCell LineageDNA GlycosylasesDNA RepairGenetic VariationGerm-Line MutationGuanineHydrocephalusMiceMice, Inbred C57BLMice, KnockoutMutationMutation RatePhosphoric Monoester HydrolasesSequence Analysis, DNA8-hydroxyguanineDNA GlycosylasesGuaninemutY adenine glycosylaseNudt1 protein, mouseOgg1 protein, mousePhosphoric Monoester Hydrolases

Identifiers

PMID24732879
PMCPMC3986730
OpenAlexW1985357654

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.