Age‐specific metabolic rates and mortality rates in the genus<i>Drosophila</i>

Promislow, Daniel E. L.; Haselkorn, Tamara S.

doi:10.1046/j.1474-9728.2002.00009.x

Cited by 72 publications

(49 citation statements)

References 55 publications

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“…As the lifespan of different Drosophila species may have different sensitivity to temperature, this may introduce further variation in the data. Indeed, several longevity studies on D. melanogaster at 25°C reported mean lifespans that were longer than we observed here: 42 days (Simon, Shih, Mack & Benzer, 2003); 55–65 days (Hercus, Loeschcke & Rattan, 2003); 59–60 days (Promislow & Haselkorn, 2002); 27–36 days on baker's yeast; and 71 days on brewer's yeast (Bass, Weinkove, Houthoofd, Gems & Partridge, 2007). This suggests that other factors such as diet might also have impacted our measured lifespans.…”

Section: Discussionsupporting

confidence: 40%

Comparative transcriptomics across 14 Drosophila species reveals signatures of longevity

Avanesov

Porter

et al. 2018

Aging Cell

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SummaryLifespan varies dramatically among species, but the biological basis is not well understood. Previous studies in model organisms revealed the importance of nutrient sensing, mTOR, NAD/sirtuins, and insulin/IGF1 signaling in lifespan control. By studying life‐history traits and transcriptomes of 14 Drosophila species differing more than sixfold in lifespan, we explored expression divergence and identified genes and processes that correlate with longevity. These longevity signatures suggested that longer‐lived flies upregulate fatty acid metabolism, downregulate neuronal system development and activin signaling, and alter dynamics of RNA splicing. Interestingly, these gene expression patterns resembled those of flies under dietary restriction and several other lifespan‐extending interventions, although on the individual gene level, there was no significant overlap with genes previously reported to have lifespan‐extension effects. We experimentally tested the lifespan regulation potential of several candidate genes and found no consistent effects, suggesting that individual genes generally do not explain the observed longevity patterns. Instead, it appears that lifespan regulation across species is modulated by complex relationships at the system level represented by global gene expression.

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Section: Discussionsupporting

confidence: 40%

Comparative transcriptomics across 14 Drosophila species reveals signatures of longevity

Avanesov

Porter

et al. 2018

Aging Cell

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“…This anomaly has been established for dogs for some time (Michell, 1999;Li et al, 1996;Patronek et al, 1997;Egenvall et al, 2000). In contrast to these data, however, several studies on different strains of Drosophila (Promislow and Haselkorn, 2002;Novoseltsev et al, 2002;Van Voorhies et al, 2003) show no relationship between energy expenditures and lifespan.…”

Section: (I) Studies Of Transgenic and Natural Mutant Animalsmentioning

confidence: 55%

Body size, energy metabolism and lifespan

Speakman

2005

Journal of Experimental Biology

758

637

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Bigger animals live longer. The scaling exponent for the relationship between lifespan and body mass is between 0.15 and 0.3. Bigger animals also expend more energy, and the scaling exponent for the relationship of resting metabolic rate (RMR) to body mass lies somewhere between 0.66 and 0.8. Mass-specific RMR therefore scales with a corresponding exponent between -0.2 and -0.33. Because the exponents for mass-specific RMR are close to the exponents for lifespan, but have opposite signs, their product (the mass-specific expenditure of energy per lifespan) is independent of body mass (exponent between -0.08 and 0.08). This means that across species a gram of tissue on average expends about the same amount of energy before it dies regardless of whether that tissue is located in a shrew, a cow, an elephant or a whale. This fact led to the notion that ageing and lifespan are processes regulated by energy metabolism rates and that elevating metabolism will be associated with premature mortalitythe rate of living theory.The free-radical theory of ageing provides a potential mechanism that links metabolism to ageing phenomena, since oxygen free radicals are formed as a by-product of oxidative phosphorylation. Despite this potential synergy in these theoretical approaches, the free-radical theory has grown in stature while the rate of living theory has fallen into disrepute. This is primarily because comparisons made across classes (for example, between birds and mammals) do not conform to the expectations, and even within classes there is substantial interspecific variability in the mass-specific expenditure of energy per lifespan. Using interspecific data to test the rate of living hypothesis is, however, confused by several major problems. For example, appeals that the resultant lifetime expenditure of energy per gram of tissue is 'too variable' depend on the biological significance rather than the statistical significance of the variation observed. Moreover, maximum lifespan is not a good marker of ageing and RMR is not a good measure of total energy metabolism. Analysis of residual lifespan against residual RMR reveals no significant relationship. However, this is still based on RMR.A novel comparison using daily energy expenditure (DEE), rather than BMR, suggests that lifetime expenditure of energy per gram of tissue is NOT independent of body mass, and that tissue in smaller animals expends more energy before expiring than tissue in larger animals. Some of the residual variation in this relationship in mammals is explained by ambient temperature. In addition there is a significant negative relationship between residual lifespan and residual daily energy expenditure in mammals. A potentially much better model to explore the links of body size, metabolism and ageing is to examine the intraspecific links. These studies have generated some data that support the original rate of living theory and other data that conflict. In particular several studies have shown that manipulating animals to expend more or less energy ...

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“…In most species of Drosophila, metabolic rates do not change with age (Promislow and Haselkorn 2002). There is no correlation between age and ROS production, and over-expression of the adenine nucleotide translocase (ANT) decreases ROS levels but shortens longevity (Miwa et al 2004).…”

Section: Discussionmentioning

confidence: 99%

“…If mitochondria are responsible for aging, it would follow that some change in metabolic rate or ROS levels in mitochondria should be detected with increasing age. However, metabolic rates do not change with age in most Drosophila species (Promislow and Haselkorn 2002). ROS levels do not change with age in D. melanogaster, and neither CR nor overexpression of adenine nucleotide translocase (important in regulating ADP transport in mitochondria) decreases ROS production (Miwa et al 2004).…”

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confidence: 99%

Nuclear–Mitochondrial Epistasis and Drosophila Aging: Introgression of Drosophila simulans mtDNA Modifies Longevity in D. melanogaster Nuclear Backgrounds

2006

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Under the mitochondrial theory of aging, physiological decline with age results from the accumulated cellular damage produced by reactive oxygen species generated during electron transport in the mitochondrion. A large body of literature has documented age-specific declines in mitochondrial function that are consistent with this theory, but relatively few studies have been able to distinguish cause from consequence in the association between mitochondrial function and aging. Since mitochondrial function is jointly encoded by mitochondrial (mtDNA) and nuclear genes, the mitochondrial genetics of aging should be controlled by variation in (1) mtDNA, (2) nuclear genes, or (3) nuclear-mtDNA interactions. The goal of this study was to assess the relative contributions of these factors in causing variation in Drosophila longevity. We compared strains of flies carrying mtDNAs with varying levels of divergence: two strains from Zimbabwe (,20 bp substitutions between mtDNAs), strains from Crete and the United States (20-40 bp substitutions between mtDNAs), and introgression strains of Drosophila melanogaster carrying mtDNA from Drosophila simulans in a D. melanogaster Oregon-R chromosomal background (.500 silent and 80 amino acid substitutions between these mtDNAs). Longevity was studied in reciprocal cross genotypes between pairs of these strains to test for cytoplasmic (mtDNA) factors affecting aging. The intrapopulation crosses between Zimbabwe strains show no difference in longevity between mtDNAs; the interpopulation crosses between Crete and the United States show subtle but significant differences in longevity; and the interspecific introgression lines showed very significant differences between mtDNAs. However, the genotypes carrying the D. simulans mtDNA were not consistently short-lived, as might be predicted from the disruption of nuclear-mitochondrial coadaptation. Rather, the interspecific mtDNA strains showed a wide range of variation that flanked the longevities seen between intraspecific mtDNAs, resulting in very significant nuclear 3 mtDNA epistatic interaction effects. These results suggest that even ''defective'' mtDNA haplotypes could extend longevity in different nuclear allelic backgrounds, which could account for the variable effects attributable to mtDNA haplogroups in human aging.

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Age‐specific metabolic rates and mortality rates in the genusDrosophila

Cited by 72 publications

References 55 publications

Comparative transcriptomics across 14 Drosophila species reveals signatures of longevity

Comparative transcriptomics across 14 Drosophila species reveals signatures of longevity

Body size, energy metabolism and lifespan

Nuclear–Mitochondrial Epistasis and Drosophila Aging: Introgression of Drosophila simulans mtDNA Modifies Longevity in D. melanogaster Nuclear Backgrounds

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