Cited by 79Genetics, Aging, and Longevity in Model OrganismsMitochondrial Function and PathologyAutophagy in Disease and Therapy

Mitochondrial free radical generation and lifespan control in the fungal aging model Podospora anserina

Gredilla, Ricardo, Grief, Jürgen, Osiewacz, Heinz D.·2006·Experimental Gerontology

Abstract

In the filamentous fungus Podospora anserina a central role of mitochondria in the control of aging has been repeatedly demonstrated. Interestingly, impairments in cytochrome c oxidase (COX) activity induce an enhancement in the expression of the quinol-oxygen alternative oxidoreductase (AOX) correlating with an extension of lifespan. This effect is thought to be determined by a reduction of the free radical generation in mitochondria. In the current investigation we have analyzed the electron transport chain composition of P. anserina and the superoxide generation rate in wild type s and in mutant grisea, a long-lived mutant with complex IV deficiency. Here we report that, similarly to other fungi, mitochondrial respiration in P. anserina is a combination of standard and alternative routes. A switch in the COX/AOX respiration balance affects the mitochondrial free radical generation. Lower mitochondrial rates of superoxide generation were found in the long-lived mutant, supporting the central role of mitochondrial free radical generation in the lifespan control of P. anserina. The question of how the activity of the alternative respiratory pathway influences the rate of free radical generation in P. anserina mitochondria is discussed.

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Crossref · 10.1016/j.exger.2006.01.010

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  • For several genotypes the Podospora anserina culture will grow for 3-5 weeks and then enter senescence marked by mitochondrial DNA instabilities, increased ROS, mitochondrial fission, accumulation of pigment and cell death.

    “For several genotypes the culture will grow for 3-5 weeks and then enter senescence marked by mitochondrial DNA instabilities, increased ROS, mitochondrial fission, accumulation of pigment and cell death (Gredilla et al., 2006; Osiewacz et al., 2010).”

    From Programmed cell death in aging (2015) · cites this paper as Gredilla et al., 2006

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References 50 · Cited by 79

Authors
Gredilla, R., Grief, J., & Osiewacz, H. D.
Affiliations
Goethe University Frankfurt (DE)
Corresponding author
Osiewacz, Heinz D.
Venue
Experimental Gerontology
Publisher
Elsevier BV
Published
2006-04
Volume
41
Issue
4
Pages
439-447
ISSN
0531-5565 (ISSN-L)
OpenAlex
W2036412806
Cited by
79
References
50
Citations by year
2026: 2 · 2024: 4 · 2022: 6 · 2021: 4 · 2017: 1 · 2016: 2 · 2015: 3 · 2014: 6 · 2013: 5 · 2012: 5
FWCI
2.47
Type
journal article
Language
en
Open access
closed
Locations
  • Experimental Gerontology (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • European Commission (LSHM-CT-2004-512020)
  • Deutsche Forschungsgemeinschaft (Os75/5-3)
  • Ministerio de Educación, Cultura y Deporte
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
Keywords
Podospora anserina, mitochondrial free radicals, superoxide production, aging, cytochrome c oxidase, alternative oxidase, electron transport chain, complex IV deficiency, mitochondrial respiration, long-lived mutants, fungal aging
MeSH terms
Aging, Free Radicals, Longevity, Mitochondria, Mycology, NADH Dehydrogenase, Oxygen Consumption, RNA, Messenger, Submitochondrial Particles, Superoxide Dismutase, Blotting, Western, Oxidative Stress, Reverse Transcriptase Polymerase Chain Reaction, Electron Transport Chain Complex Proteins, Podospora

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