scholarly journals Enhanced stress-induced senescence-response may increase species lifespan

Aging ◽  
2021 ◽  
Author(s):  
Antonello Lorenzini ◽  
Christian Sell
Keyword(s):  
Species Lifespan

scholarly journals DNA Methylation Networks Underlying Mammalian Traits

2021 ◽  
Author(s):  
A. Haghani ◽  
A.T. Lu ◽  
C.Z. Li ◽  
T.R. Robeck ◽  
K. Belov ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Growth Hormone ◽  
Phylogenetic Tree ◽  
Hormone Receptors ◽  
Tissue Type ◽  
Mammalian Evolution ◽  
Order Analysis ◽  
Species Lifespan ◽  
Different Tissues

SummaryEpigenetics has hitherto been studied and understood largely at the level of individual organisms. Here, we report a multi-faceted investigation of DNA methylation across 11,117 samples from 176 different species. We performed an unbiased clustering of individual cytosines into 55 modules and identified 31 modules related to primary traits including age, species lifespan, sex, adult species weight, tissue type and phylogenetic order. Analysis of the correlation between DNA methylation and species allowed us to construct phyloepigenetic trees for different tissues that parallel the phylogenetic tree. In addition, while some stable cytosines reflect phylogenetic signatures, others relate to age and lifespan, and in many cases responding to anti-aging interventions in mice such as caloric restriction and ablation of growth hormone receptors. Insights uncovered by this investigation have important implications for our understanding of the role of epigenetics in mammalian evolution, aging and lifespan.

scholarly journals Epidemics as an adaptive driving force determining lifespan setpoints

2020 ◽  
Vol 117 (30) ◽  
pp. 17937-17948
Author(s):  
Peter V. Lidsky ◽  
Raul Andino
Keyword(s):  
Life Expectancy ◽  
Genetic Control ◽  
Driving Force ◽  
Driving Forces ◽  
New Host ◽  
Species Specific ◽  
Pathogen Clearance ◽  
The Impact ◽  
Species Lifespan ◽  
Infection Spread

Species-specific limits to lifespan (lifespan setpoint) determine the life expectancy of any given organism. Whether limiting lifespan provides an evolutionary benefit or is the result of an inevitable decline in fitness remains controversial. The identification of mutations extending lifespan suggests that aging is under genetic control, but the evolutionary driving forces limiting lifespan have not been defined. By examining the impact of lifespan on pathogen spread in a population, we propose that epidemics drive lifespan setpoints’ evolution. Shorter lifespan limits infection spread and accelerates pathogen clearance when compared to populations with longer-lived individuals. Limiting longevity is particularly beneficial in the context of zoonotic transmissions, where pathogens must undergo adaptation to a new host. Strikingly, in populations exposed to pathogens, shorter-living variants outcompete individuals with longer lifespans. We submit that infection outbreaks can contribute to control the evolution of species’ lifespan setpoints.

scholarly journals Evolution of telomere maintenance and tumour suppressor mechanisms across mammals

2018 ◽  
Vol 373 (1741) ◽  
pp. 20160443 ◽  
Author(s):  
Xiao Tian ◽  
Katherine Doerig ◽  
Rosa Park ◽  
Alice Can Ran Qin ◽  
Chaewon Hwang ◽  
...  
Keyword(s):  
Replicative Senescence ◽  
Mammalian Species ◽  
Telomerase Activity ◽  
Tumour Suppressor ◽  
Telomere Maintenance ◽  
Large Species ◽  
Increased Risk ◽  
Telomere Biology ◽  
Risk Of Cancer ◽  
Species Lifespan

Mammalian species differ dramatically in telomere biology. Species larger than 5–10 kg repress somatic telomerase activity and have shorter telomeres, leading to replicative senescence. It has been proposed that evolution of replicative senescence in large-bodied species is an anti-tumour mechanism counteracting increased risk of cancer due to increased cell numbers. By contrast, small-bodied species express high telomerase activity and have longer telomeres. To counteract cancer risk due to longer lifespan, long-lived small-bodied species evolved additional telomere-independent tumour suppressor mechanisms. Here, we tested the connection between telomere biology and tumorigenesis by analysing the propensity of fibroblasts from 18 rodent species to form tumours. We found a negative correlation between species lifespan and anchorage-independent growth. Small-bodied species required inactivation of Rb and/or p53 and expression of oncogenic H-Ras to form tumours. Large-bodied species displayed a continuum of phenotypes requiring additional genetic ‘hits’ for malignant transformation. Based on these data we refine the model of the evolution of tumour suppressor mechanisms and telomeres. We propose that two different strategies evolved in small and large species because small-bodied species cannot tolerate small tumours that form prior to activation of the telomere barrier, and must instead use telomere-independent strategies that act earlier, at the hyperplasia stage. This article is part of the theme issue ‘Understanding diversity in telomere dynamics’.

scholarly journals Evolution of Natural Lifespan Variation and Molecular Strategies of Extended Lifespan

2020 ◽  
Author(s):  
Alaattin Kaya ◽  
Cheryl Zi Jin Phua ◽  
Mitchell Lee ◽  
Lu Wang ◽  
Alexander Tyshkovskiy ◽  
...  
Keyword(s):  
Genetic Basis ◽  
Epigenetic Landscape ◽  
Intermediary Metabolites ◽  
Closely Related Species ◽  
Nad Metabolism ◽  
Lifespan Variation ◽  
Extended Lifespan ◽  
Selective Forces ◽  
Biology Of Aging ◽  
Species Lifespan

ABSTRACTThe question of why and how some species or individuals within a population live longer than others is among the most important questions in the biology of aging. A particularly useful model to understand the genetic basis and selective forces acting on the plasticity of lifespan are closely related species or ecologically diverse individuals of the same species widely different in lifespan. Here, we analyzed 76 diverse wild isolates of two closely related budding yeast species Saccharomyces cerevisiae and Saccharomyces paradoxus and discovered a diversity of natural intra-species lifespan variation. We sequenced the genomes of these organisms and analyzed how their replicative lifespan is shaped by nutrients and transcriptional and metabolite patterns. We identified sets of genes and metabolites to regulate aging pathways, many of which have not been previously associated with lifespan regulation. We also identified and characterized long-lived strains with elevated intermediary metabolites and differentially regulated genes for NAD metabolism and the control of epigenetic landscape through chromatin silencing. Our data further offer insights into the evolution and mechanisms by which caloric restriction regulates lifespan by modulating the availability of nutrients without decreasing fitness. Overall, our study shows how the environment and natural selection interact to shape diversity of lifespan.

scholarly journals Sensitivity of primary fibroblasts in culture to atmospheric oxygen does not correlate with species lifespan

Aging ◽  
2016 ◽  
Vol 8 (5) ◽  
pp. 841-847 ◽  
Author(s):  
Alison Patrick ◽  
Michael Seluanov ◽  
Chaewon Hwang ◽  
Jonathan Tam ◽  
Tanya Khan ◽  
...  
Keyword(s):  
Atmospheric Oxygen ◽  
Primary Fibroblasts ◽  
Species Lifespan

scholarly journals Within-individual repeatability in telomere length: a meta-analysis in non-mammalian vertebrates

2021 ◽  
Author(s):  
Tiia Kärkkäinen ◽  
Michael Briga ◽  
Toni Laaksonen ◽  
Antoine Stier
Keyword(s):  
Telomere Length ◽  
Phylogenetic Signal ◽  
Meta Analysis ◽  
Biological Factors ◽  
Long Term Outcomes ◽  
Term Survival ◽  
High Repeatability ◽  
Individual Repeatability ◽  
Species Lifespan

Telomere length is increasingly used as a biomarker of long-term life history costs, ageing and future survival prospects. Yet, to have the potential to predict long-term outcomes, telomere length should exhibit a relatively high within-individual repeatability over time, which has been largely overlooked in past studies. To fill this gap, we conducted a meta-analysis on 74 studies reporting longitudinal telomere length assessment in non-mammalian vertebrates, with the aim to establish the current pattern of within-individual repeatability in telomere length and to identify the methodological (e.g. qPCR/TRF, study length) and biological factors (e.g. taxon, wild/captive, age class, species lifespan, phylogeny) that may affect it. While the median within-individual repeatability of telomere length was moderate to high (R = 0.55; 95% CI: 0.05-0.95; N = 82), marked heterogeneity between studies was evident. Measurement method affected strongly repeatability estimate, with TRF-based studies exhibiting high repeatability (R = 0.80; 95% CI: 0.34-0.96; N = 25), while repeatability of qPCR-based studies was only half of that and more variable (R = 0.46; 95% CI: 0.04-0.82; N = 57). While phylogeny explained some variance in repeatability, phylogenetic signal was not significant (λ = 0.32; 95% CI: 0.00-0.83). None of the biological factors investigated here had a statistically significant association with the repeatability of telomere length, being potentially obscured by methodological noise. Our meta-analysis highlights the need to carefully evaluate and consider within-individual repeatability in telomere studies to ensure the robustness of using telomere length as a biomarker of long-term survival and fitness prospects.

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