Evidence map›Paper›PMID 17407571›Full record

ArticleBMC genetics2007

A mitochondrial mutator plasmid that causes senescence under dietary restricted conditions.

Marc F P M Maas, Rolf F Hoekstra, Alfons J M Debets

Abstract read
In one paragraph

Article in BMC genetics, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Article
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.

Marc F P M MaasCentre de Génétique Moléculaire, Centre Nationale de la Recherche Scientifique, Gif-sur-Yvette, France. Maas@cgm.cnrs-gif.fr
Rolf F Hoekstra
Alfons J M Debets

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCalorie or dietary restriction extends life span in a wide range of organisms including the filamentous fungus Podospora anserina. Under dietary restricted conditions, P. anserina isolates are several-fold longer lived. This is however not the case in isolates that carry one of the pAL2-1 homologous mitochondrial plasmids.

resultsWe show that the pAL2-1 homologues act as 'insertional mutators' of the mitochondrial genome, which may explain their negative effect on life span extension. Sequencing revealed at least fourteen unique plasmid integration sites, of which twelve were located within the mitochondrial genome and two within copies of the plasmid itself. The plasmids were able to integrate in their entirety, via a non-homologous mode of recombination. Some of the integrated plasmid copies were truncated, which probably resulted from secondary, post-integrative, recombination processes. Integration sites were predominantly located within and surrounding the region containing the mitochondrial rDNA loci.

conclusionWe propose a model for the mechanism of integration, based on innate modes of mtDNA recombination, and discuss its possible link with the plasmid's negative effect on dietary restriction mediated life span extension.

Indexed as

Mutagenesis, InsertionalPlasmidsCaloric RestrictionCulture MediaDNA, FungalDNA, MitochondrialPodosporaPolymerase Chain ReactionPolymorphism, Restriction Fragment LengthRecombination, GeneticCulture MediaDNA, FungalDNA, Mitochondrial

Identifiers

PMID17407571
PMCPMC1864894

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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.