The mitochondrial plasmid pAL2-1 reduces calorie restriction mediated life span extension in the filamentous fungus Podospora anserina

Calorie restriction is the only life span extending regimen known that applies to all aging organisms. Although most fungi do not appear to senesce, all natural isolates of the modular filamentous fungus Podospora anserina have a limited life span. In this paper, we show that calorie restriction ext...

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Bibliographic Details
Published in:Fungal genetics and biology 2004-09, Vol.41 (9), p.865-871
Main Authors: Maas, Marc F.P.M, Boer, Hugo J.de, Debets, Alfons J.M, Hoekstra, Rolf F
Format: Article
Language:English
Subjects:
Ageing
Caloric Restriction
dna
DNA, Fungal - genetics
DNA, Fungal - physiology
DNA, Mitochondrial - genetics
DNA, Mitochondrial - physiology
dynamics
Energy Intake
Energy Metabolism
Extrachromosomal Inheritance - genetics
Extrachromosomal Inheritance - physiology
Fungal senescence
Invertron
Linear mitochondrial plasmid
longevity
Mitochondria - genetics
mutant
organisms
Plasmids
Podospora anserina
senescence
Sordariales - genetics
Sordariales - physiology
Submitochondrial Particles
Time Factors
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Summary:Calorie restriction is the only life span extending regimen known that applies to all aging organisms. Although most fungi do not appear to senesce, all natural isolates of the modular filamentous fungus Podospora anserina have a limited life span. In this paper, we show that calorie restriction extends life span also in Podospora anserina. The response to glucose limitation varies significantly among 23 natural isolates from a local population in The Netherlands, ranging from no effect up to a 5-fold life span extension. The isolate dependent effect is largely due to the presence or absence of pAL2-1 homologous plasmids. These mitochondrial plasmids are associated with reduced life span under calorie restricted conditions, suggesting a causal link. This has been substantiated using three combinations of isogenic isolates with and without plasmids. A model is proposed to explain how pAL2-1 homologues influence the response to calorie restriction.
ISSN:1087-1845
1096-0937
DOI:10.1016/j.fgb.2004.04.007