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.
Highlights
Calorie or dietary restriction extends life span in a wide range of organisms including the filamentous fungus Podospora anserina
We 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 (DR) mediated life span extension
PAL2-1 homologues abrogate the life span extending response to dietary restriction We have previously shown that Podospora anserina responds to glucose restriction in a highly strain-dependent manner [7]
Summary
Calorie or dietary restriction extends life span in a wide range of organisms including the filamentous fungus Podospora anserina. Calorie or dietary restriction (DR) extends life span in a wide range of organisms. In recent years several important nutrient-sensitive cellular signalling pathways have been discovered, which are at least partially conserved between organisms, e.g. the insulin/ IGF-1-like and TOR (target of rapamycin) mediated signalling pathways [1,2,3]. These are involved in adjusting cellular metabolism to nutrient availability. At the proximate level DR appears to act by adjusting cellular metabolism to a mode set for survival
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