Accumulation of linear mitochondrial DNA fragments in the nucleus shortens the chronological life span of yeast

2012 ◽  
Vol 91 (10) ◽  
pp. 782-788 ◽  
Author(s):  
Xin Cheng ◽  
Andreas S. Ivessa
Keyword(s):  
Mitochondrial Dna ◽  
Life Span ◽  
Dna Fragments ◽  
Chronological Life Span ◽  
Linear Mitochondrial Dna

SOD2 Functions Downstream of Sch9 to Extend Longevity in Yeast

Genetics ◽  
2003 ◽  
Vol 163 (1) ◽  
pp. 35-46 ◽  
Author(s):  
Paola Fabrizio ◽  
Lee-Loung Liou ◽  
Vanessa N Moy ◽  
Alberto Diaspro ◽  
Joan Selverstone Valentine ◽  
...  
Keyword(s):  
Life Span ◽  
Stress Resistance ◽  
Reversible Inactivation ◽  
Life Span Extension ◽  
Resistance Proteins ◽  
Mitochondrial Superoxide ◽  
Mitochondrial Aconitase ◽  
Chronological Life Span ◽  
Survival Extension ◽  
Mitochondrial Superoxide Dismutase

Abstract Signal transduction pathways inactivated during periods of starvation are implicated in the regulation of longevity in organisms ranging from yeast to mammals, but the mechanisms responsible for life-span extension are poorly understood. Chronological life-span extension in S. cerevisiae cyr1 and sch9 mutants is mediated by the stress-resistance proteins Msn2/Msn4 and Rim15. Here we show that mitochondrial superoxide dismutase (Sod2) is required for survival extension in yeast. Deletion of SOD2 abolishes life-span extension in sch9Δ mutants and decreases survival in cyr1:mTn mutants. The overexpression of Sods—mitochondrial Sod2 and cytosolic CuZnSod (Sod1)—delays the age-dependent reversible inactivation of mitochondrial aconitase, a superoxide-sensitive enzyme, and extends survival by 30%. Deletion of the RAS2 gene, which functions upstream of CYR1, also doubles the mean life span by a mechanism that requires Msn2/4 and Sod2. These findings link mutations that extend chronological life span in S. cerevisiae to superoxide dismutases and suggest that the induction of other stress-resistance genes regulated by Msn2/4 and Rim15 is required for maximum longevity extension.

Ecl1 is a zinc-binding protein involved in the zinc-limitation-dependent extension of chronological life span in fission yeast

2017 ◽  
Vol 292 (2) ◽  
pp. 475-481 ◽  
Author(s):  
Takafumi Shimasaki ◽  
Hokuto Ohtsuka ◽  
Chikako Naito ◽  
Kenko Azuma ◽  
Takeshi Tenno ◽  
...  
Keyword(s):  
Life Span ◽  
Fission Yeast ◽  
Binding Protein ◽  
Zinc Binding ◽  
Chronological Life Span

Magnolol protects Saccharomyces cerevisiae antioxidant-deficient mutants from oxidative stress and extends yeast chronological life span

2019 ◽  
Vol 366 (8) ◽  
Author(s):  
Subasri Subramaniyan ◽  
Phaniendra Alugoju ◽  
Sudharshan SJ ◽  
Bhavana Veerabhadrappa ◽  
Madhu Dyavaiah
Keyword(s):  
Oxidative Stress ◽  
Saccharomyces Cerevisiae ◽  
Life Span ◽  
Chronological Life Span

scholarly journals Do mitochondrial DNA fragments promote cancer and aging?

FEBS Letters ◽  
1988 ◽  
Vol 241 (1-2) ◽  
pp. 1-5 ◽  
Author(s):  
Christoph Richter
Keyword(s):  
Mitochondrial Dna ◽  
Dna Fragments

scholarly journals Mitochondrial Respiratory Thresholds Regulate Yeast Chronological Life Span and its Extension by Caloric Restriction

2012 ◽  
Vol 16 (1) ◽  
pp. 55-67 ◽  
Author(s):  
Alejandro Ocampo ◽  
Jingjing Liu ◽  
Elizabeth A. Schroeder ◽  
Gerald S. Shadel ◽  
Antoni Barrientos
Keyword(s):  
Life Span ◽  
Caloric Restriction ◽  
Chronological Life Span ◽  
Mitochondrial Respiratory

scholarly journals Two Copies of mthmg1, Encoding a Novel Mitochondrial HMG-Like Protein, Delay Accumulation of Mitochondrial DNA Deletions in Podospora anserina

2002 ◽  
Vol 1 (4) ◽  
pp. 503-513 ◽  
Author(s):  
Michelle Dequard-Chablat ◽  
Cynthia Alland
Keyword(s):  
Mitochondrial Dna ◽  
Dna Binding ◽  
Mitochondrial Genome ◽  
Life Span ◽  
Cellular Localization ◽  
Premature Death ◽  
Podospora Anserina ◽  
Protein Fusion ◽  
Dna Binding Domains ◽  
Binding Domains

ABSTRACT In the filamentous fungus Podospora anserina, two degenerative processes which result in growth arrest are associated with mitochondrial genome (mitochondrial DNA [mtDNA]) instability. Senescence is correlated with mtDNA rearrangements and amplification of specific regions (senDNAs). Premature death syndrome is characterized by the accumulation of specific mtDNA deletions. This accumulation is due to indirect effects of the AS1-4 mutation, which alters a cytosolic ribosomal protein gene. The mthmg1 gene has been identified as a double-copy suppressor of premature death. It greatly delays premature death and the accumulation of deletions when it is present in two copies in an AS1-4 context. The duplication of mthmg1 has no significant effect on the wild-type life span or on senDNA patterns. In an AS1 + context, deletion of the mthmg1 gene alters germination, growth, and fertility and reduces the life span. The Δmthmg1 senescent strains display a particular senDNA pattern. This deletion is lethal in an AS1-4 context. According to its physical properties (very basic protein with putative mitochondrial targeting sequence and HMG-type DNA-binding domains) and the cellular localization of an mtHMG1-green fluorescent protein fusion, mtHMG1 appears to be a mitochondrial protein possibly associated with mtDNA. It is noteworthy that it is the first example of a protein combining the two DNA-binding domains, AT-hook motif and HMG-1 boxes. It may be involved in the stability and/or transmission of the mitochondrial genome. To date, no structural homologues have been found in other organisms. However, mtHMG1 displays functional similarities with the Saccharomyces cerevisiae mitochondrial HMG-box protein Abf2.

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