Evidence map›Paper›PMID 24864316›Full record

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

Regular bottlenecks and restrictions to somatic fusion prevent the accumulation of mitochondrial defects in Neurospora.

E Bastiaans, D K Aanen, A J M Debets, R F Hoekstra, B Lestrade, M F P M Maas

Abstract read
In one paragraph

Article 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 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
2.8field-weighted citation impact, top 9% 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, 26 citations in OpenAlex.

  1. Review
  2. Mitigation of age-dependent accumulation of defective mitochondrial genomes.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  3. Syncytia in Fungi.Cells · 2020
    Review
  4. Intracellular quality control of mitochondrial DNA: evidence and limitations.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2020
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. What cost mitochondria? The maintenance of functional mitochondrial DNA within and across generations.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2014
    Review
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 2 institutions in 2 countries.

E BastiaansLaboratory of Genetics, Wageningen University, Droevendaalsesteeg 1, Wageningen 6708 PB, The Netherlands eric.bastiaans@wur.nl.
D K AanenLaboratory of Genetics, Wageningen University, Droevendaalsesteeg 1, Wageningen 6708 PB, The Netherlands.
A J M DebetsLaboratory of Genetics, Wageningen University, Droevendaalsesteeg 1, Wageningen 6708 PB, The Netherlands.
R F HoekstraLaboratory of Genetics, Wageningen University, Droevendaalsesteeg 1, Wageningen 6708 PB, The Netherlands.
B LestradeLaboratory of Genetics, Wageningen University, Droevendaalsesteeg 1, Wageningen 6708 PB, The Netherlands.
M F P M MaasLaboratory of Genetics, Wageningen University, Droevendaalsesteeg 1, Wageningen 6708 PB, The Netherlands.
Wageningen University & Research · NLGoogle (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The replication and segregation of multi-copy mitochondrial DNA (mtDNA) are not under strict control of the nuclear DNA. Within-cell selection may thus favour variants with an intracellular selective advantage but a detrimental effect on cell fitness. High relatedness among the mtDNA variants of an individual is predicted to disfavour such deleterious selfish genetic elements, but experimental evidence for this hypothesis is scarce. We studied the effect of mtDNA relatedness on the opportunities for suppressive mtDNA variants in the fungus Neurospora carrying the mitochondrial mutator plasmid pKALILO. During growth, this plasmid integrates into the mitochondrial genome, generating suppressive mtDNA variants. These mtDNA variants gradually replace the wild-type mtDNA, ultimately culminating in growth arrest and death. We show that regular sequestration of mtDNA variation is required for effective selection against suppressive mtDNA variants. First, bottlenecks in the number of mtDNA copies from which a 'Kalilo' culture started significantly increased the maximum lifespan and variation in lifespan among cultures. Second, restrictions to somatic fusion among fungal individuals, either by using anastomosis-deficient mutants or by generating allotype diversity, prevented the accumulation of suppressive mtDNA variants. We discuss the implications of these results for the somatic accumulation of mitochondrial defects during ageing.

Indexed as

Genetic VariationSelection, GeneticAgingDNA, MitochondrialDNA ReplicationMitochondriaMutagenesis, InsertionalNeurosporaDNA, Mitochondrialanastomosiskin selectionlevels of selectionmitochondriamulti-level selectionsenescence

Identifiers

PMID24864316
PMCPMC4032522
OpenAlexW2168107110

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.