The short-lived fish Nothobranchius furzeri as a new model system for aging studies

Terzibasi, Eva; Valenzano, Dario Riccardo; Cellerino, Alessandro

doi:10.1016/j.exger.2006.06.039

Cited by 122 publications

(88 citation statements)

References 81 publications

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“…One of the predictions from the classical aging theory suggests that low levels of extrinsic hazards should lead to the evolution of slow aging, whereas high extrinsic mortality should result in fast aging (Austad & Kirkwood, 2008). Consistent with this theory, previous studies have shown that the short lifespan of N. furzeri is associated with fast aging such as an early onset of aging biomarkers (e.g., lipofuscin accumulation and b-galactosidase activity), a decline in learning ⁄ behavioural capabilities and age-related telomere shortening (Terzibasi et al, 2007(Terzibasi et al, , 2008Hartmann et al, 2009). In this study, we addressed the questions of whether different aspects of mitochondria biology are affected during aging of N. furzeri.…”

Section: Introductionmentioning

confidence: 58%

“…This is the shortest reported maximum lifespan of a vertebrate that can be bred in captivity (Valdesalici & Cellerino, 2003). N. furzeri is therefore emerging as an alternative model organism for age research (Terzibasi et al, 2007). The natural habitat of N. furzeri is seasonal ponds in south-east Africa, which are filled with water during the rainy season, and N. furzeri survives the dry season in form of protected eggs.…”

Section: Introductionmentioning

confidence: 99%

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Mitochondrial DNA copy number and function decrease with age in the short‐lived fish Nothobranchius furzeri

et al. 2011

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SummaryAmong vertebrates that can be kept in captivity, the annual fish Nothobranchius furzeri possesses the shortest known lifespan. It also shows typical signs of aging and is therefore an ideal model to assess the role of different physiological and environmental parameters on aging and lifespan determination. Here, we used Nothobranchius furzeri to study whether aging is associated with mitochondrial DNA (mtDNA) alterations and changes in mitochondrial function. We sequenced the complete mitochondrial genome of N. furzeri and found an extended control region. Large-scale mtDNA deletions have been frequently described to accumulate in other organisms with age, but there was no evidence for the presence of detectable age-related mtDNA deletions in N. furzeri. However, mtDNA copy number significantly decreased with age in skeletal muscle, brain, liver, skin and dorsal fin. Consistent with this finding, expression of Pgc-1a that encodes a transcriptional coactivator of mitochondrial biogenesis and expression of Tfam and mtSsbp both encoding mtDNA binding factors was downregulated with age. The investigation of possible changes in mitochondrial function revealed that the content of respiratory chain complexes III and IV was reduced in skeletal muscle with age. In addition, ADP-stimulated and succinate-dependent respiration was decreased in mitochondria of old fish. These findings suggest that despite the short lifespan, aging in N. furzeri is associated with a decline in mtDNA copy number, the downregulation of mtDNA-associated genes and an impairment of mitochondrial function.

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Section: Introductionmentioning

confidence: 58%

Section: Introductionmentioning

confidence: 99%

Mitochondrial DNA copy number and function decrease with age in the short‐lived fish Nothobranchius furzeri

et al. 2011

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“…Indeed, despite their short lifespan compared to other vertebrates, various strains of the turquoise killifish recapitulate numerous stereotypical aging traits that have been reported in other vertebrates (Figure 5), including decline in reproduction, fertility, cognition, mobility, regeneration, and tissue homeostasis, along with increased incidence of senescence, neural and muscular degeneration, and cancerous lesions (Di Cicco et al., 2011; Terzibasi, Valenzano & Cellerino, 2007; Terzibasi et al., 2008; Valenzano, Terzibasi, Cattaneo, Domenici & Cellerino, 2006; Wendler, Hartmann, Hoppe & Englert, 2015). Importantly, the turquoise killifish does not die of just one disease, but appears to have multiple causes of death in old age, indicating that its lifespan is truly compressed rather than limited by a specific disease.…”

Section: The African Turquoise Killifish Lifecycle Is Composed Of Twomentioning

confidence: 99%

The African turquoise killifish: A research organism to study vertebrate aging and diapause

Brunet²

2018

Aging Cell

135

118

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SummaryThe African turquoise killifish has recently gained significant traction as a new research organism in the aging field. Our understanding of aging has strongly benefited from canonical research organisms—yeast, C. elegans, Drosophila, zebrafish, and mice. Many characteristics that are essential to understand aging—for example, the adaptive immune system or the hypothalamo‐pituitary axis—are only present in vertebrates (zebrafish and mice). However, zebrafish and mice live more than 3 years and their relatively long lifespans are not compatible with high‐throughput studies. Therefore, the turquoise killifish, a vertebrate with a naturally compressed lifespan of only 4–6 months, fills an essential gap to understand aging. With a recently developed genomic and genetic toolkit, the turquoise killifish not only provides practical advantages for lifespan and longitudinal experiments, but also allows more systematic characterizations of the interplay between genetics and environment during vertebrate aging. Interestingly, the turquoise killifish can also enter a long‐term dormant state during development called diapause. Killifish embryos in diapause already have some organs and tissues, and they can last in this state for years, exhibiting exceptional resistance to stress and to damages due to the passage of time. Understanding the diapause state could give new insights into strategies to prevent the damage caused by aging and to better preserve organs, tissues, and cells. Thus, the African turquoise killifish brings two interesting aspects to the aging field—a compressed lifespan and a long‐term resistant diapause state, both of which should spark new discoveries in the field.

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“…Resveratrol was shown to extend the life span in Drosophila (Griswold et al 2008) and C. elegans (Gruber et al 2007) as well as in vertebrates such as short-lived fish Northobranchius (Terzibasi et al 2007). Bauer et al showed for the first time that resveratrol could extend life span in case of mammals also , In this study, high-calorie diets (60% of calories from fat) induced obesity, triggering an inflammatory response and comorbidities, such as diabetes and atherosclerosis, which decreased the life span in case of middle-aged (1-yearold) mice, but resveratrol treatment (22.4 mg/kg/day) along with the high-fat diets extended the life span by inducing Sirt1 similar to calorierestricted animals with greater SIRT1 coexpression (Nisoli et al 2005).…”

Section: Resveratrol and Longevitymentioning

confidence: 99%

Dose-Dependency of Resveratrol in Providing Health Benefits

2010

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The short-lived fish Nothobranchius furzeri as a new model system for aging studies

Cited by 122 publications

References 81 publications

Mitochondrial DNA copy number and function decrease with age in the short‐lived fish Nothobranchius furzeri

Mitochondrial DNA copy number and function decrease with age in the short‐lived fish Nothobranchius furzeri

The African turquoise killifish: A research organism to study vertebrate aging and diapause

Dose-Dependency of Resveratrol in Providing Health Benefits

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