Evidence map›Paper›PMID 24614072›Full record

ArticleNature genetics2014

Selective propagation of functional mitochondrial DNA during oogenesis restricts the transmission of a deleterious mitochondrial variant.

Jahda H Hill, Zhe Chen, Hong Xu

Open access · greenAbstract read
In one paragraph

Article in Nature genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 117 papers.

0numbers the graph read from it
0cells of the map it votes in
117citing papers in PubMed
8.0field-weighted citation impact, top 2% 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

117 citing papers in PubMed, 196 citations in OpenAlex.

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  13. Mitochondrial curation for the next generation.Current opinion in genetics & development · 2025
    Review
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57 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

3 authors at 2 institutions in 1 country.

Jahda H Hill1] Laboratory of Molecular Genetics, National Heart, Lung, and Blood Institute, US National Institutes of Health, Bethesda, Maryland, USA. [2].
Zhe Chen1] Laboratory of Molecular Genetics, National Heart, Lung, and Blood Institute, US National Institutes of Health, Bethesda, Maryland, USA. [2].
Hong XuLaboratory of Molecular Genetics, National Heart, Lung, and Blood Institute, US National Institutes of Health, Bethesda, Maryland, USA.
National Heart Lung and Blood Institute · USNational Institutes of Health · US

Funding

Mitochondrial DNA inheritance in DrosophilaZIAHL006153 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI XU, HONG · 2012 to 2025
$26.5M
Mitochondrial Genetics and PhysiologyZIAHL006096 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI XU, HONG · 2011 to 2011
$2.5M
Intramural NIH HHS ZIA HL006096Intramural NIH HHS ZIA HL006153
6 · The paper itself

Abstract

Although mitochondrial DNA (mtDNA) is prone to mutation and few mtDNA repair mechanisms exist, crippling mitochondrial mutations are exceedingly rare. Recent studies have demonstrated strong purifying selection in the mouse female germline. However, the mechanisms underlying positive selection of healthy mitochondria remain to be elucidated. We visualized mtDNA replication during Drosophila melanogaster oogenesis, finding that mtDNA replication commenced before oocyte determination during the late germarium stage and was dependent on mitochondrial fitness. We isolated a temperature-sensitive lethal mtDNA allele, mt:CoI(T300I), which resulted in reduced mtDNA replication in the germarium at the restrictive temperature. Additionally, the frequency of the mt:CoI(T300I) allele in heteroplasmic flies was decreased, both during oogenesis and over multiple generations, at the restrictive temperature. Furthermore, we determined that selection against mt:CoI(T300I) overlaps with the timing of selective replication of mtDNA in the germarium. These findings establish a previously uncharacterized developmental mechanism for the selective amplification of wild-type mtDNA, which may be evolutionarily conserved to limit the transmission of deleterious mutations.

Indexed as

Evolution, MolecularAnimalsCarbonyl Cyanide p-TrifluoromethoxyphenylhydrazoneDNA, MitochondrialDNA ReplicationDrosophila melanogasterFemaleGenes, LethalModels, GeneticOogenesisSelection, GeneticTemperatureTime FactorsCarbonyl Cyanide p-TrifluoromethoxyphenylhydrazoneDNA, Mitochondrial

Identifiers

PMID24614072
PMCPMC3976679
OpenAlexW2017363253

What OpenQuestion holds

Textmetadata
LicenceTDM
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.