Evidence map›Paper›PMID 27009201›Full record

ArticleMolecular biology of the cell2016

Reactive oxygen species stimulate mitochondrial allele segregation toward homoplasmy in human cells.

Feng Ling, Rong Niu, Hideyuki Hatakeyama, Yu-Ichi Goto, Takehiko Shibata, Minoru Yoshida

Abstract read
In one paragraph

Article in Molecular biology of the cell, 2016. 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
1.2field-weighted citation impact, top 20% 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, 21 citations in OpenAlex.

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  12. Mitochondrial DNA Mutations Induced by Carbon Ions Radiation: A Preliminary Study.Dose-response : a publication of International Hormesis Society
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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

6 authors at 1 institution in 1 country.

Feng LingChemical Genetics Laboratory, RIKEN, Saitama 351-0198, Japan Japan Agency for Medical Research and Development-Core Research for Evolutional Science and Technology, Tokyo 100-0004 Japan ling@postman.riken.go.jp tshibata@postman.riken.go.jp.
Rong NiuChemical Genetics Laboratory, RIKEN, Saitama 351-0198, Japan Japan Agency for Medical Research and Development-Core Research for Evolutional Science and Technology, Tokyo 100-0004 Japan.
Hideyuki HatakeyamaJapan Agency for Medical Research and Development-Core Research for Evolutional Science and Technology, Tokyo 100-0004 Japan Department of Mental Retardation and Birth Defect Research, National Center of Neurology and Psychiatry, Tokyo 187-8502, Japan.
Yu-Ichi GotoJapan Agency for Medical Research and Development-Core Research for Evolutional Science and Technology, Tokyo 100-0004 Japan Department of Mental Retardation and Birth Defect Research, National Center of Neurology and Psychiatry, Tokyo 187-8502, Japan.
Takehiko ShibataJapan Agency for Medical Research and Development-Core Research for Evolutional Science and Technology, Tokyo 100-0004 Japan Cellular and Molecular Biology Laboratory, RIKEN, Saitama 351-0198, Japan ling@postman.riken.go.jp tshibata@postman.riken.go.jp.
Minoru YoshidaChemical Genetics Laboratory, RIKEN, Saitama 351-0198, Japan Japan Agency for Medical Research and Development-Core Research for Evolutional Science and Technology, Tokyo 100-0004 Japan.
Japan Agency for Medical Research and Development · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondria that contain a mixture of mutant and wild-type mitochondrial (mt) DNA copies are heteroplasmic. In humans, homoplasmy is restored during early oogenesis and reprogramming of somatic cells, but the mechanism of mt-allele segregation remains unknown. In budding yeast, homoplasmy is restored by head-to-tail concatemer formation in mother cells by reactive oxygen species (ROS)-induced rolling-circle replication and selective transmission of concatemers to daughter cells, but this mechanism is not obvious in higher eukaryotes. Here, using heteroplasmic m.3243A > G primary fibroblast cells derived from MELAS patients treated with hydrogen peroxide (H2O2), we show that an optimal ROS level promotes mt-allele segregation toward wild-type and mutant mtDNA homoplasmy. Enhanced ROS level reduced the amount of intact mtDNA replication templates but increased linear tandem multimers linked by head-to-tail unit-sized mtDNA (mtDNA concatemers). ROS-triggered mt-allele segregation correlated with mtDNA-concatemer production and enabled transmission of multiple identical mt-genome copies as a single unit. Our results support a mechanism by which mt-allele segregation toward mt-homoplasmy is mediated by concatemers.

Indexed as

AllelesChromosome SegregationDNA, MitochondrialDNA ReplicationFibroblastsGenes, MitochondrialGenome, MitochondrialHumansMELAS SyndromeMitochondriaMutationPrimary Cell CultureReactive Oxygen SpeciesDNA, MitochondrialReactive Oxygen Species

Identifiers

PMID27009201
PMCPMC4865324
OpenAlexW2407756956

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.