Evidence map›Paper›PMID 24864309›Full record

ReviewPhilosophical transactions of the Royal Society of London. Series B, Biological sciences2014

What cost mitochondria? The maintenance of functional mitochondrial DNA within and across generations.

Duur K Aanen, Johannes N Spelbrink, Madeleine Beekman

Abstract readReview
In one paragraph

Review in Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

23 citing papers in PubMed, 61 citations in OpenAlex.

  1. Article
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  3. Review
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  5. Review
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  7. Review
  8. Article
  9. Review
  10. Linking the mitochondrial genotype to phenotype: a complex endeavour.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2020
    Article
  11. Maternal transmission of mitochondrial diseases.Genetics and molecular biology · 2020
    Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
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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

3 authors at 3 institutions in 3 countries.

Duur K AanenLaboratory of Genetics, Wageningen University, Droevendaalsesteeg 1, PO Box 309, 6700 AH Wageningen, The Netherlands duur.aanen@wur.nl.
Johannes N SpelbrinkDepartment of Pediatrics, Nijmegen Centre for Mitochondrial Disorders, Radboud University Medical Centre, Geert Grooteplein 10, PO Box 9101, 6500 HB Nijmegen, The Netherlands FinMIT Centre of Excellence, BioMediTech and Tampere University Hospital, Pirkanmaa Hospital District, 33014 Tampere, Finland.
Madeleine BeekmanBehaviour and Genetics of Social Insects Lab, The University of Sydney, Sydney NSW 2006, Australia.
Pirkanmaa Hospital District · FIUniversity of Sydney · AUWageningen University & Research · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The peculiar biology of mitochondrial DNA (mtDNA) potentially has detrimental consequences for organismal health and lifespan. Typically, eukaryotic cells contain multiple mitochondria, each with multiple mtDNA genomes. The high copy number of mtDNA implies that selection on mtDNA functionality is relaxed. Furthermore, because mtDNA replication is not strictly regulated, within-cell selection may favour mtDNA variants with a replication advantage, but a deleterious effect on cell fitness. The opportunities for selfish mtDNA mutations to spread are restricted by various organism-level adaptations, such as uniparental transmission, germline mtDNA bottlenecks, germline selection and, during somatic growth, regular alternation between fusion and fission of mitochondria. These mechanisms are all hypothesized to maintain functional mtDNA. However, the strength of selection for maintenance of functional mtDNA progressively declines with age, resulting in age-related diseases. Furthermore, organismal adaptations that most probably evolved to restrict the opportunities for selfish mtDNA create secondary problems. Owing to predominantly maternal mtDNA transmission, recombination among mtDNA from different individuals is highly restricted or absent, reducing the scope for repair. Moreover, maternal inheritance precludes selection against mtDNA variants with male-specific effects. We finish by discussing the consequences of life-history differences among taxa with respect to mtDNA evolution and make a case for the use of microorganisms to experimentally manipulate levels of selection.

Indexed as

Biological EvolutionSelection, GeneticAnimalsDNA, MitochondrialDNA ReplicationHumansMitochondriaMutationDNA, Mitochondrialevolutiongenetic conflictmitochondriamitochondrial diseasemitochondrial DNA

Identifiers

PMID24864309
PMCPMC4032515
OpenAlexW2159003778

What OpenQuestion holds

Textmetadata
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.