Mitochondrial Proteins

Publication Title: 
Biogerontology

P. anserina mutants with impairments in complex IV (COX) of the respiratory chain are characterized by an increase in lifespan. Examples are the nuclear grisea mutant with a moderate lifespan extension (60%) and the immortal extranuclear ex1 mutant. Here we report data demonstrating that in mutant ex1 the level of the alternative oxidase (PaAOX) is significantly higher than in mutant grisea. PaAOX levels appear to be reversely dependent on COX activity.

Author(s): 
Borghouts, Corina
Scheckhuber, Christian Q.
Werner, Alexandra
Osiewacz, Heinz D.
Publication Title: 
Experimental Cell Research

The lifespan of human foreskin fibroblasts (HFF5), cultured under standard in vitro conditions (including ambient atmospheric oxygen tension), was extended slightly by expression of exogenous mortalin (mot-2)/mthsp70/Grp75, but not by the catalytic subunit of telomerase, hTERT. Together, mot-2 and hTERT permitted bypass of senescence, a substantial extension of lifespan, and possibly immortalization. This is the first demonstration that mot-2 and telomerase can cooperate in the immortalization process.

Author(s): 
Kaul, Sunil C.
Yaguchi, Tomoko
Taira, Kazunari
Reddel, Roger R.
Wadhwa, Renu
Publication Title: 
Experimental Gerontology

Uncoupling proteins (UCPs) can dissipate mitochondrial protonmotive force by increasing the proton conductance of the inner membrane and through this effect could decrease ROS production, ameliorate oxidative stress and extend lifespan. We investigated whether ubiquitous, pan-neuronal or neurosecretory cell-specific expression of human UCP3 (hUCP3) in adult Drosophila melanogaster affected lifespan.

Author(s): 
Humphrey, Dickon M.
Toivonen, Janne M.
Giannakou, Maria
Partridge, Linda
Brand, Martin D.
Publication Title: 
Experimental Gerontology

As in the case of aging, many degenerative disorders also result from progressive mitochondrial deterioration and cellular damage accumulation. Therefore, preventing damage accumulation may delay aging and help to prevent degenerative disorders, especially those associated with mitochondrial dysfunction. In the nematode Caenorhabditis elegans a mild mitochondrial dysfunction prolongs the lifespan.

Author(s): 
Torgovnick, Alessandro
Schiavi, Alfonso
Testi, Roberto
Ventura, Natascia
Publication Title: 
Mechanisms of Ageing and Development

The quest to understand why we age has given rise to numerous lines of investigation that have gradually converged to include metabolic control by mitochondrial activity as a major player. That is, the ideal balance between nutrient uptake, its transduction into usable energy, and the mitigation of damaging byproducts can be regulated by mitochondrial respiration and output (ATP, reactive oxygen species (ROS), and heat). Mitochondrial inefficiency through proton leak, which uncouples substrate oxidation from ADP phosphorylation, can comprise as much as 30% of the basal metabolic rate.

Author(s): 
Mookerjee, Shona A.
Divakaruni, Ajit S.
Jastroch, Martin
Brand, Martin D.
Publication Title: 
Experimental Gerontology

The brown fat specific UnCoupling Protein 1 (UCP1) is involved in thermogenesis, a process by which energy is dissipated as heat in response to cold stress and excess of caloric intake. Thermogenesis has potential implications for body mass control and cellular fat metabolism. In fact, in humans, the variability of the UCP1 gene is associated with obesity, fat gain and metabolism. Since regulation of metabolism is one of the key-pathways in lifespan extension, we tested the possible effects of UCP1 variability on survival.

Author(s): 
Rose, Giuseppina
Crocco, Paolina
D'Aquila, Patrizia
Montesanto, Alberto
Bellizzi, Dina
Passarino, Giuseppe
Publication Title: 
Antioxidants & Redox Signaling

SIGNIFICANCE: Among the most highly investigated theories of aging is the mitochondrial theory of aging. The basis of this theory includes a central role for altered or compromised mitochondrial function in the pathophysiologic declines associated with aging. In general, studies in various organisms, including nematodes, rodents, and humans, have largely upheld that aging is associated with mitochondrial dysfunction.

Author(s): 
Pulliam, Daniel A.
Bhattacharya, Arunabh
Van Remmen, Holly
Publication Title: 
Nature

The naked mole rat (Heterocephalus glaber) is a strictly subterranean, extraordinarily long-lived eusocial mammal. Although it is the size of a mouse, its maximum lifespan exceeds 30 years, making this animal the longest-living rodent. Naked mole rats show negligible senescence, no age-related increase in mortality, and high fecundity until death. In addition to delayed ageing, they are resistant to both spontaneous cancer and experimentally induced tumorigenesis. Naked mole rats pose a challenge to the theories that link ageing, cancer and redox homeostasis.

Author(s): 
Kim, Eun Bae
Fang, Xiaodong
Fushan, Alexey A.
Huang, Zhiyong
Lobanov, Alexei V.
Han, Lijuan
Marino, Stefano M.
Sun, Xiaoqing
Turanov, Anton A.
Yang, Pengcheng
Yim, Sun Hee
Zhao, Xiang
Kasaikina, Marina V.
Stoletzki, Nina
Peng, Chunfang
Polak, Paz
Xiong, Zhiqiang
Kiezun, Adam
Zhu, Yabing
Chen, Yuanxin
Kryukov, Gregory V.
Zhang, Qiang
Peshkin, Leonid
Yang, Lan
Bronson, Roderick T.
Buffenstein, Rochelle
Wang, Bo
Han, Changlei
Li, Qiye
Chen, Li
Zhao, Wei
Sunyaev, Shamil R.
Park, Thomas J.
Zhang, Guojie
Wang, Jun
Gladyshev, Vadim N.
Publication Title: 
PLoS biology

An increasing number of genes required for mitochondrial biogenesis, dynamics, or function have been found to be mutated in metabolic disorders and neurological diseases such as Leigh Syndrome. In a forward genetic screen to identify genes required for neuronal function and survival in Drosophila photoreceptor neurons, we have identified mutations in the mitochondrial methionyl-tRNA synthetase, Aats-met, the homologue of human MARS2. The fly mutants exhibit age-dependent degeneration of photoreceptors, shortened lifespan, and reduced cell proliferation in epithelial tissues.

Author(s): 
Bayat, Vafa
Thiffault, Isabelle
Jaiswal, Manish
TÈtreault, Martine
Donti, Taraka
Sasarman, Florin
Bernard, GeneviËve
Demers-Lamarche, Julie
Dicaire, Marie-JosÈe
Mathieu, Jean
Vanasse, Michel
Bouchard, Jean-Pierre
Rioux, Marie-France
Lourenco, Charles M.
Li, Zhihong
Haueter, Claire
Shoubridge, Eric A.
Graham, Brett H.
Brais, Bernard
Bellen, Hugo J.
Publication Title: 
PloS One

The human gene C10orf2 encodes the mitochondrial replicative DNA helicase Twinkle, mutations of which are responsible for a significant fraction of cases of autosomal dominant progressive external ophthalmoplegia (adPEO), a human mitochondrial disease caused by defects in intergenomic communication. We report the analysis of orthologous mutations in the Drosophila melanogaster mitochondrial DNA (mtDNA) helicase gene, d-mtDNA helicase.

Author(s): 
Sanchez-Martinez, Alvaro
Calleja, Manuel
Peralta, Susana
Matsushima, Yuichi
Hernandez-Sierra, Rosana
Whitworth, Alexander J.
Kaguni, Laurie S.
Garesse, Rafael

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