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

Maas, Marc F.P.M.; Boer, Hugo J. de; Debets, A.J.M.; Hoekstra, Rolf F.

doi:10.1016/j.fgb.2004.04.007

Cited by 32 publications

(38 citation statements)

References 24 publications

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“…While it is impossible to highlight all such studies, it is worth noting that a simple reduction of available glucose in the media results in life extension in P. anserina (Maas et al 2004) and in yeast (Lin et al 2000). More relevant to our discussion is that, in S. cerevisiae, a metabolic shift from glucose metabolism and fermentation toward respiration plays a central part in this life extension (Lin et al 2002).…”

Section: G303smentioning

confidence: 99%

Mutations in Two Zinc-Cluster Proteins Activate Alternative Respiratory and Gluconeogenic Pathways and Restore Senescence in Long-Lived Respiratory Mutants ofPodospora anserina

et al. 2009

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In Podospora anserina, inactivation of the respiratory chain results in a spectacular life-span extension. This inactivation is accompanied by the induction of the alternative oxidase. Although the functional value of this response is evident, the mechanism behind it is far from understood. By screening suppressors able to reduce the life-span extension of cytochrome-deficient mutants, we identified mutations in two zinc-cluster proteins, RSE2 and RSE3, which are conserved in other ascomycetes. These mutations led to the overexpression of the genes encoding the alternative oxidase and the gluconeogenic enzymes, fructose-1, 6 biphosphatase, and pyruvate carboxykinase. Both RSE2 and RSE3 are required for the expression of these genes. We also show that, even in the absence of a respiratory deficiency, the wild-type RSE2 and RSE3 transcription factors are involved in life-span control and their inactivation retards aging. These data are discussed with respect to aging, the regulation of the alternative oxidase, and carbon metabolism.

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Section: G303smentioning

confidence: 99%

Mutations in Two Zinc-Cluster Proteins Activate Alternative Respiratory and Gluconeogenic Pathways and Restore Senescence in Long-Lived Respiratory Mutants ofPodospora anserina

et al. 2009

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“…Moreover, also the invertron-type plasmid pAL2-1 from P. anserina shortens life span without any notable beneficial effects on reproduction (Maas et al 2004). Thus there appears to be no trade-off between life span and reproduction with regard to plasmid-based senescence, contrary to expectations from evolutionary explanations of aging.…”

Section: Discussionmentioning

confidence: 84%

“…Thus there appears to be no trade-off between life span and reproduction with regard to plasmid-based senescence, contrary to expectations from evolutionary explanations of aging. Furthermore, plasmid-based senescence does not appear to respond to calorie restriction in a life-span-extending manner as it does in all other aging organisms (Maas et al 2004). It is thus probably best seen as a lethal disease.…”

Section: Discussionmentioning

confidence: 99%

Hybrid Mitochondrial Plasmids From Senescence Suppressor Isolates of Neurospora intermedia

2007

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We analyzed several natural suppressor isolates of the pKalilo-based fungal senescence syndrome of Neurospora intermedia. The pKalilo plasmid did not increase in titer in these isolates. Nor did it show integration ''de novo.'' In at least two of the senescence suppressor isolates, pKalilo had formed stable recombinants with other mitochondrial elements. pKalilo/mtDNA recombination junctions were complete and appeared to have been formed via a nonhomologous recombination mechanism. Further analysis revealed that pKalilo had recombined a novel, 2.6-kb cryptic mitochondrial retroplasmid, similar to the mitochondrial retroplasmid pTHR1 from Trichoderma harzianum and retroplasmids of the ''Varkud'' homology group. The recombinant molecules consisted of pKalilo, the novel element, and short intervening stretches of mtDNA. The latter stretches clearly corresponded to ''in vivo'' mitochondrial cDNA, suggesting that the molecules had formed via the action of a template-switching reverse transcriptase. We discuss how different types of mitochondrial plasmids interact and how their detrimental effect on the host may be suppressed.

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“…Integration of pAL2-1 homologues and the life span extending response to DR PAL2-1 was originally considered a longevity plasmid [19], later a neutral plasmid [6] and more recently a senescence plasmid [7]. This can be explained by the fact that other senescence processes normally overshadow the effects of 'plasmid-based' senescence in Podospora, so that only those cases come to light in which the integration of plasmids is associated with longevity.…”

Section: Discussionmentioning

confidence: 99%

“…The plasmid is sometimes lost in the sexual cycle though, and plasmid-carrying isolates can thus be 'cured'. These 'cured' isolates respond adequately to DR [7], suggesting a causal relationship between the presence of the plasmids and the abrogation of life span extension under DR conditions. PAL2-1 is a mitochondrial plasmid of the 'invertron'-type [8].…”

Section: Introductionmentioning

confidence: 93%

A mitochondrial mutator plasmid that causes senescence under dietary restricted conditions

2007

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

Cited by 32 publications

References 24 publications

Mutations in Two Zinc-Cluster Proteins Activate Alternative Respiratory and Gluconeogenic Pathways and Restore Senescence in Long-Lived Respiratory Mutants ofPodospora anserina

Mutations in Two Zinc-Cluster Proteins Activate Alternative Respiratory and Gluconeogenic Pathways and Restore Senescence in Long-Lived Respiratory Mutants ofPodospora anserina

Hybrid Mitochondrial Plasmids From Senescence Suppressor Isolates of Neurospora intermedia

A mitochondrial mutator plasmid that causes senescence under dietary restricted conditions

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