Long-lived Animals Research Articles

Naked mole rats activate neuroprotective proteins during hypoxia.

Naked mole rats are a long-lived animal model that age much like humans, but that can also withstand oxidative damage, cancer, neurodegenerative diseases, and severe hypoxic conditions, which is of particular interest to this study. The conditions of their underground burrows result in competition for oxygen consumption, yet despite this oxygen deprivation they emerge unscathed. To understand the mechanisms in place to facilitate neuronal preservation during hypoxia, we investigated the protein levels of well-known cell-stress factors. We found that under hypoxic conditions, nearly half of the proteins measured increased expression in brain, while only a few decreased. Under hypoxic conditions there appeared to be a HIF1α-centered response, where HIF1α and its interactors carbonic anhydrase 9, CITED2, p21/CIP1, and NFκB1, among others, were upregulated. Concurrently, a hypoxia-induced decrease of cytochrome c was consistent with decreased mitochondrial function and protection from apoptosis. The picture that emerges is one of neuroprotection, cell-cycle arrest, and the promotion of antiapoptotic functions, all of which are consistent with conserving energy and maintaining neural integrity under low oxygen levels. These results suggest how this species may be poised to face hypoxia and contribute to its remarkable ability to deal with myriad of other damaging factors and sets the stage for future work on the neuroprotective facilitators we identified.

Developmental responses to early-life adversity: Evolutionary and mechanistic perspectives.

Adverse ecological and social conditions during early life are known to influence development, with rippling effects that may explain variation in adult health and fitness. The adaptive function of such developmental plasticity, however, remains relatively untested in long-lived animals, resulting in much debate over which evolutionary models are most applicable. Furthermore, despite the promise of clinical interventions that might alleviate the health consequences of early-life adversity, research on the proximate mechanisms governing phenotypic responses to adversity have been largely limited to studies on glucocorticoids. Here, we synthesize the current state of research on developmental plasticity, discussing both ultimate and proximate mechanisms. First, we evaluate the utility of adaptive models proposed to explain developmental responses to early-life adversity, particularly for long-lived mammals such as humans. In doing so, we highlight how parent-offspring conflict complicates our understanding of whether mothers or offspring benefit from these responses. Second, we discuss the role of glucocorticoids and a second physiological system-the gut microbiome-that has emerged as an additional, clinically relevant mechanism by which early-life adversity can influence development. Finally, we suggest ways in which nonhuman primates can serve as models to study the effects of early-life adversity, both from evolutionary and clinical perspectives.

Long-lived animals with negligible senescence: clues for ageing research.

Among several theories to explain the complicated process of human ageing, the mitochondrial oxidative stress hypothesis has received recent attention. Considering that lifespan and ageing rates vary considerably across taxa, a better understanding of factors that lead to negligible or extremely rapid senescence in mammals may generate novel approaches to target human ageing. Several species, such as naked mole rats, ocean quahog, rockfish and Greenland shark, have been identified that exhibit negligible senescence and superior resistance to age-related diseases. Considering that the available literature suggests that their outstanding stress resistance is linked to maintenance of protein homeostasis and robust mitochondrial functions, treatments that target protein modification and upregulation of matrix antioxidants may have implications for extending human health span.

Persistent remodeling and neurodegeneration in late-stage retinal degeneration.

Retinal remodeling is a progressive series of negative plasticity revisions that arise from retinal degeneration, and are seen in retinitis pigmentosa, age-related macular degeneration and other forms of retinal disease. These processes occur regardless of the precipitating event leading to degeneration. Retinal remodeling then culminates in a late-stage neurodegeneration that is indistinguishable from progressive central nervous system (CNS) proteinopathies. Following long-term deafferentation from photoreceptor cell death in humans, and long-lived animal models of retinal degeneration, most retinal neurons reprogram, then die. Glial cells reprogram into multiple anomalous metabolic phenotypes. At the same time, survivor neurons display degenerative inclusions that appear identical to progressive CNS neurodegenerative disease, and contain aberrant α-synuclein (α-syn) and phosphorylated α-syn. In addition, ultrastructural analysis indicates a novel potential mechanism for misfolded protein transfer that may explain how proteinopathies spread. While neurodegeneration poses a barrier to prospective retinal interventions that target primary photoreceptor loss, understanding the progression and time-course of retinal remodeling will be essential for the establishment of windows of therapeutic intervention and appropriate tuning and design of interventions. Finally, the development of protein aggregates and widespread neurodegeneration in numerous retinal degenerative diseases positions the retina as a ideal platform for the study of proteinopathies, and mechanisms of neurodegeneration that drive devastating CNS diseases.

An ontogenetic perspective on migratory strategy of a long‐lived pelagic seabird: Timings and destinations change progressively during maturation

The processes that drive the ontogeny of migratory strategies in long-lived animals with slow maturation remain enigmatic. While some short-lived migrants are known or believed to repeat the same migratory patterns throughout their lives, little is known on the time required for immature long-lived migrants to progressively acquire adult-like migratory behaviours, or which aspects take longer to refine during the maturation process. Here, we studied the ontogeny of long-distance migratory strategies and related patterns of spatial distribution in a long-lived seabird species during the annual cycle. To do so, we deployed light-level geolocators on 4- to 9-year-old immature Cory's shearwaters (Calonectris borealis) and on breeding adults. We revealed that migratory timings and destinations of young shearwaters progressively changed with age. The effect of ageing was remarkably evident on spring migratory performance and phenology. Birds gradually shortened the duration of the non-breeding period by advancing departure date and reducing travelling time, which resulted in a sequential arrival at the colony of the various age contingents. Ageing immatures gradually changed from a more exploratory strategy to a more conservative way of exploiting resources, reducing both their year-round spatial spread across oceanic domains and the total distance travelled. Immatures always performed a trans-equatorial migration to the Southern Hemisphere, contrasting with 17% of the adults which remained in the North Atlantic year-round. Finally, during the breeding season immatures were widely dispersed through the North Atlantic reducing their overlap with breeding adults. Our long-term study provides empirical support to the hypothesis that in long-lived species, the refinement of migratory behaviour and year-round spatial distribution is a progressive process mediated by age and experience, where life stage constraints and competition for resources may also play a role. The emerging pattern suggests that for some avian taxa, the ontogeny of migratory strategy is a prolonged, complex and dynamic process.

In-Vivo Quantitative Image Analysis of Age-Related Morphological Changes of C. elegans Neurons Reveals a Correlation between Neurite Bending and Novel Neurite Outgrowths.

The aging of the human brain in the absence of diseases is accompanied by subtle changes of neuronal morphology, such as dendrite restructuring, neuronal sprouting, and synaptic deteriorations, rather than neurodegeneration or gross deterioration. Similarly, the nervous system of Caenorhabditis elegans does not show neurodegeneration or gross deterioration during normal aging, but displays subtle alterations in neuronal morphology. The occurrence of these age-dependent abnormalities is stochastic and dynamic, which poses a major challenge to fully capture them for quantitative comparison. Here, we developed a semi-automated pipeline for quantitative image analysis of these features during aging. We employed and evaluated this pipeline herein to reproduce findings from previous studies using visual inspection of neuronal morphology. Importantly, our approach can also quantify additional features, such as soma volume, the length of neurite outgrowths, and their location along the aged neuron. We found that, during aging, the soma of neurons decreases in volume, whereas the number and length of neurite outgrowths from the soma both increase. Long-lived animals showed less decrease in soma volume, fewer and shorter neurite outgrowths, and protection against abnormal sharp bends preferentially localized at the distal part of the dendrites during aging. We found a correlation of sharp bends with neurite outgrowth, suggesting the hypothesis that sharp bends might proceed neurite outgrowths. Thus, our semi-automated pipeline can help researchers to obtain and analyze quantitative datasets of this stochastic process for comparison across genotypes and to identify correlations to facilitate the generation of novel hypothesis.

Multiple stable isotopes identify sediment organic matter as the primary nutritional source to American brook lamprey larvae along a stream gradient

Multiple stable isotope ratios (δ2H, δ13C, δ15N, and δ34S) of American brook lamprey (Lethenteron appendix) ammocoetes and their potential sources were measured along a stream gradient. Isotopic ratios were successful at differentiating three potential sources: terrestrial organic matter (TOM; upland plants), sediment organic matter (SOM; benthic organic material), and algae. Bayesian mixing models (MixSIAR) utilizing δ13C, δ15N, and δ34S estimated ammocoetes were highly reliant on SOM at all sites (>95%), but inclusion of δ2H increased the importance of both algae and model uncertainty. Ammocoete δ2H was more depleted than anticipated even after lipid extraction and after accounting for trophic water contributions, suggesting δ2H in consumer tissues (especially for long-lived animals) is still incompletely understood. Model sensitivity testing with trophic fractionation values did not substantially change the results. Regardless of the mixing model investigated, none indicated more algae in ammocoete diets in downstream rather than upstream sites, in contrast with expectations about river productivity. Stable isotopes suggest SOM, and not algae, is nutritionally most important to ammocoetes, even in downstream reaches of rivers.

Muscle fiber structure in an aging long-lived seabird, the black-legged kittiwake (Rissa tridactyla).

Many long-lived animals do not appear to show classic signs of aging, perhaps because they show negligible senescence until dying from "catastrophic" mortality. Muscle senescence is seldom examined in wild animals, yet decline in muscle function is one of the first signs of aging in many lab animals and humans. Seabirds are an excellent study system for physiological implications of aging because they are long-lived animals that actively forage and reproduce in the wild. Here, we examined linkages between pectoralis muscle fiber structure and age in black-legged kittiwakes (Rissa tridactyla). Pectoralis muscle is the largest organ complex in birds, and responsible for flight and shivering. We obtained and fixed biopsies from wild black-legged kittiwakes of known age. We then measured muscle fiber diameter, myonuclear domain and capillaries per fiber area among birds of differing ages. All muscle parameters were independent of age. Number of nuclei per mm of fiber showed a positive correlation with muscle fiber cross-sectional area, and myonuclear domain increased with muscle fiber diameter. Thus, as muscle fibers increased in size, they may not have recruited satellite cells, increasing the protein turnover load per nuclei. We conclude that senescence in a long-lived bird with an active lifestyle, does not entail mammalian-like changes in muscle structure.

Return to the Sea, Get Huge, Beat Cancer: An Analysis of Cetacean Genomes Including an Assembly for the Humpback Whale (Megaptera novaeangliae).

Cetaceans are a clade of highly specialized aquatic mammals that include the largest animals that have ever lived. The largest whales can have ∼1,000× more cells than a human, with long lifespans, leaving them theoretically susceptible to cancer. However, large-bodied and long-lived animals do not suffer higher risks of cancer mortality than humans—an observation known as Peto’s Paradox. To investigate the genomic bases of gigantism and other cetacean adaptations, we generated a de novo genome assembly for the humpback whale (Megaptera novaeangliae) and incorporated the genomes of ten cetacean species in a comparative analysis. We found further evidence that rorquals (family Balaenopteridae) radiated during the Miocene or earlier, and inferred that perturbations in abundance and/or the interocean connectivity of North Atlantic humpback whale populations likely occurred throughout the Pleistocene. Our comparative genomic results suggest that the evolution of cetacean gigantism was accompanied by strong selection on pathways that are directly linked to cancer. Large segmental duplications in whale genomes contained genes controlling the apoptotic pathway, and genes inferred to be under accelerated evolution and positive selection in cetaceans were enriched for biological processes such as cell cycle checkpoint, cell signaling, and proliferation. We also inferred positive selection on genes controlling the mammalian appendicular and cranial skeletal elements in the cetacean lineage, which are relevant to extensive anatomical changes during cetacean evolution. Genomic analyses shed light on the molecular mechanisms underlying cetacean traits, including gigantism, and will contribute to the development of future targets for human cancer therapies.

Metal concentrations in archaeological and contemporary mussel shells (Unionidae): Reconstruction of past environmental conditions and the present state

Freshwater mussels are widely used in the monitoring of pollution because they are filter-feeding, long-lived animals that tend to accumulate metals in their shells. The temporal scale of such studies can reach thousands of years, since the composition of shells preserves them against decay. This allows us to reconstruct past environmental conditions and to compare current environmental conditions to those prevalent thousands of years ago. Here we assessed metal concentrations (Ca, Cd, Cr, Cu, Fe, Hg, Ni, Pb and Zn) in recently harvested mussel shells and mussel shells found by archaeologists, and tested the hypothesis that levels of some metals are higher in today's shells, reflecting increasing anthropogenic impact. We observed lower metal concentrations (with the exception of Cd) in shells found by archaeologists (n = 35) than in recently harvested mussel shells (n = 14) (Unio crassus, Unio pictorum, Unio tumidus) in the same water bodies. There were no significant differences in metal levels among species in shells found by archaeologists, while in recently harvested mussels almost all metals for which we tested were found in their highest levels in Unio crassus. The results suggest that metal concentrations in prehistoric times were lower than today, which probably reflects human impact, rather than changes in the geochemical structure of rocks. The results also revealed that metal transfer between mussel shells and surrounding deposits does not occur. We therefore suggest that they might be successfully used as independent bioindicators.

More frequent extreme climate events stabilize reindeer population dynamics

Extreme climate events often cause population crashes but are difficult to account for in population-dynamic studies. Especially in long-lived animals, density dependence and demography may induce lagged impacts of perturbations on population growth. In Arctic ungulates, extreme rain-on-snow and ice-locked pastures have led to severe population crashes, indicating that increasingly frequent rain-on-snow events could destabilize populations. Here, using empirically parameterized, stochastic population models for High-Arctic wild reindeer, we show that more frequent rain-on-snow events actually reduce extinction risk and stabilize population dynamics due to interactions with age structure and density dependence. Extreme rain-on-snow events mainly suppress vital rates of vulnerable ages at high population densities, resulting in a crash and a new population state with resilient ages and reduced population sensitivity to subsequent icy winters. Thus, observed responses to single extreme events are poor predictors of population dynamics and persistence because internal density-dependent feedbacks act as a buffer against more frequent events.

Trophy hunting mediates sex‐specific associations between early‐life environmental conditions and adult mortality in bighorn sheep

Environmental conditions during early development, from conception to sexual maturity, can have lasting consequences on fitness components. Although adult life span often accounts for much of the variation in fitness in long-lived animals, we know little about how early environment affects adult life span in the wild, and even less about whether these effects differ between the sexes. Using data collected over 45years from wild bighorn sheep (Ovis canadensis), we investigated the effects of early environment on adult mortality in both sexes, distinguishing between natural and anthropogenic sources of mortality. We used the average body mass of yearlings (at about 15months of age) as a yearly index of environmental quality. We first examined sex differences in natural mortality responses to early environment by censoring harvested males in the year they were shot. We then investigated sex differences in the effects of early environment on overall mortality (natural and hunting mortality combined). Finally, we used path analysis to separate the direct influence of early environment from indirect influences, mediated by age at first reproduction, adult mass and horn length. As early environmental conditions improved, natural adult mortality decreased in both sexes, although for males the effect was not statistically supported. Sex differences in the effects of early environment on adult mortality were detected only when natural and hunting mortality were pooled. Males that experienced favourable early environment had longer horns as adults and died earlier because of trophy hunting, which does not mimic natural mortality. Females that experienced favourable early environment started to reproduce earlier and early primiparity was associated with reduced mortality, suggesting a silver-spoon effect. Our results show that early conditions affect males and females differently because of trophy hunting. These findings highlight the importance of considering natural and anthropogenic environmental factors across different life stages to understand sex differences in mortality.

JNK modifies neuronal metabolism to promote proteostasis and longevity.

Aging is associated with a progressive loss of tissue and metabolic homeostasis. This loss can be delayed by single‐gene perturbations, increasing lifespan. How such perturbations affect metabolic and proteostatic networks to extend lifespan remains unclear. Here, we address this question by comprehensively characterizing age‐related changes in protein turnover rates in the Drosophila brain, as well as changes in the neuronal metabolome, transcriptome, and carbon flux in long‐lived animals with elevated Jun‐N‐terminal Kinase signaling. We find that these animals exhibit a delayed age‐related decline in protein turnover rates, as well as decreased steady‐state neuronal glucose‐6‐phosphate levels and elevated carbon flux into the pentose phosphate pathway due to the induction of glucose‐6‐phosphate dehydrogenase (G6PD). Over‐expressing G6PD in neurons is sufficient to phenocopy these metabolic and proteostatic changes, as well as extend lifespan. Our study identifies a link between metabolic changes and improved proteostasis in neurons that contributes to the lifespan extension in long‐lived mutants.

Solving Peto’s Paradox to better understand cancer

Cancer is as ancient as multicellularity itself. But not all animals get cancer at the same rate. Some, such as elephants and naked mole rats, rarely get it at all, whereas others, such as ferrets and dogs, have cancer at unusually high rates. The question is why. Despite their size and lifespan, elephants are able to stave off cancer by having 20 copies of the tumor suppressor gene TP53 and 11 extra copies of LIF. Image credit: Shutterstock.com/ronnybas frimages. In 1977, British epidemiologist Richard Peto reasoned that the cells in large-bodied, long-lived animals undergo more cell divisions, and every cell division carries a small but nonnegligible risk of introducing mutations in the daughter cells. Some of those mutations could lead to cancer. So all else being equal, one would expect that large-bodied, long-lived animals would have a greater risk of cancer than small, short-lived ones. But when Peto looked into cancer incidence in some of these animals, that’s not what he found. This seemingly counterintuitive phenomenon was dubbed Peto’s paradox (1). To unravel the mystery of Peto’s paradox, researchers are studying the genome sequences of animals across the tree of life, especially those that are particularly large or particularly long-lived. But there’s no one answer. Every species studied so far seems to have solved this paradox in a different way, possibly because of different life histories and evolutionary selective pressures. Such work could offer leads for treating or preventing human cancers, says Joshua Schiffman, a pediatric oncologist at the Huntsman Cancer Institute at the University of Utah. His research shows that the set of genes and signaling pathways that are deficient or broken in patients with a high genetic risk of cancer are actually the same ones that are protecting the animals (2). “Now we can say, ‘Nature has …

Brood Size Affects Future Reproduction in a Long-Lived Bird with Precocial Young.

Estimation of trade-offs between current reproduction and future survival and fecundity of long-lived vertebrates is essential to understanding factors that shape optimal reproductive investment. Black brant geese (Branta bernicla nigricans) fledge more goslings, on average, when their broods are experimentally enlarged to be greater than the most common clutch size of four eggs. Thus, we hypothesized that the lesser frequency of brant clutches exceeding four eggs results, at least partially, from a future reduction in survival, breeding probability, or clutch size for females tending larger broods. We used an 8-year mark-recapture data set (Barker robust design) with 5 years of clutch and brood manipulations to estimate long-term consequences of reproductive decisions in brant. We did not find evidence of a trade-off between reproductive effort and true survival or future initiation date and clutch size. Rather, future breeding probability was maximized ( [SE]) for manipulated females tending broods of four goslings and was lower for females tending smaller (one gosling; [SE]) or larger (seven goslings; [SE]) broods. Our results suggest that demographic trade-offs for female brant tending large broods may reduce the fitness value of clutches larger than four and, therefore, contribute to the paucity of larger clutches. The lack of a trade-off between reproductive effort and survival provides evidence that survival, to which fitness is most sensitive in long-lived animals, is buffered against temporal variation in brant.

Population dynamics of the endangered Kemp’s ridley sea turtle following the 2010 oil spill in the Gulf of Mexico: Simulation of potential cause-effect relationships

The Kemp’s ridley (Lepidochelys kempii) is a critically endangered sea turtle that breeds nearly exclusively in the Gulf of Mexico, with scattered nesting along the U.S. Atlantic coast. In 2010, an unprecedented increase in strandings concomitant with a large oil spill in the northern Gulf raised concern about impacts on population recovery. We used several versions of an age-structured model representing hypothesized “pulse,” “press,” and “density-dependent remigration” effects of the 2010 mortality event to simulate post-2010 population dynamics. Only a “density-dependent remigration” version simulated population fluctuations observed from 2009 to 2014. Population dynamics projected through 2035 using this version indicated essentially exponential growth, with the simulated adult female population reaching ≈110,000 in 2035 (as indicated by nest counts at the index beach). Of most interest within a management context is the apparent resiliency of the population to large mortality events of short duration. Two important caveats to this statement are the assumptions that there has been no reduction of suitable habitats and that per capita availability of food resources is sufficient to support population recovery. Simulation results also provide insight into the myriad of potential responses of an age-structured population of long-lived animals to such events.

Aging and Proteins: What Does Proteostasis Have to Do with Age?

The world is aging and we must face the challenges that this brings. One of the reasons for the increasing aging of the world's population is the increase in life expectancy and, since we live longer, it is of paramount importance to live well and to prevent age-associated diseases. In this way, it is crucial to improve knowledge of the aging process and of the mechanisms that contribute to it. Ideally it would be of great interest to have a panel of biomarkers of healthy aging that would allow an estimate of the biological age of an individual. One of the changes that greatly contribute to aging is the loss of protein homeostasis, also called proteostasis. To ensure the proper function of cells and to maintain cellular proteostasis, organisms have developed systems to control protein synthesis, folding and degradation. Loss or dysfunction of proteostasis is at the root of many well-studied human neurological diseases, such as Alzheimer's disease and, more recently, it has been implicated in the aging process with some reports showing long-lived animals to have improved proteostasis. Growing evidence suggests a strong link between modifications in the quantity and/or activity of several players involved in proteostasis and longevity. In this review, we give an overview of the main characteristics of aging with focus on proteostasis. We present how changes in components of proteostasis, during aging, impact the lifespan of model organisms. We also briefly review the current state of aging biomarkers and discuss the potential of proteostasis network components as markers of healthy aging.

Redox Signaling of NADPH Oxidases Regulates Oxidative Stress Responses, Immunity and Aging.

An accumulating body of evidence suggests that transient or physiological reactive oxygen species (ROS) generated by nicotinamide adenine dinucleotide phosphate (NADPH) oxidases act as a redox signal to re-establish homeostasis. The capacity to re-establish homeostasis progressively declines during aging but is maintained in long-lived animals to promote healthy aging. In the model organism Caenorhabditis elegans, ROS generated by dual oxidases (Duox) are important for extracellular matrix integrity, pathogen defense, oxidative stress resistance, and longevity. The Duox enzymatic activity is tightly regulated and under cellular control. Developmental molting cycles, pathogen infections, toxins, mitochondrial-derived ROS, drugs, and small GTPases (e.g., RHO-1) can activate Duox (BLI-3) to generate ROS, whereas NADPH oxidase inhibitors and negative regulators, such as MEMO-1, can inhibit Duox from generating ROS. Three mechanisms-of-action have been discovered for the Duox/BLI-3-generated ROS: (1) enzymatic activity to catalyze crosslinking of free tyrosine ethyl ester in collagen bundles to stabilize extracellular matrices, (2) high ROS bursts/levels to kill pathogens, and (3) redox signaling activating downstream kinase cascades to transcription factors orchestrating oxidative stress and immunity responses to re-establish homeostasis. Although Duox function at the cell surface is well established, recent genetic and biochemical data also suggests a novel role for Duoxs at the endoplasmic reticulum membrane to control redox signaling. Evidence underlying these mechanisms initiated by ROS from NADPH oxidases, and their relevance for human aging, are discussed in this review. Appropriately controlling NADPH oxidase activity for local and physiological redox signaling to maintain cellular homeostasis might be a therapeutic strategy to promote healthy aging.

Clonal expansion of mitochondrial DNA deletions is a private mechanism of aging in long-lived animals.

Disruption of mitochondrial metabolism and loss of mitochondrial DNA (mtDNA) integrity are widely considered as evolutionarily conserved (public) mechanisms of aging (López‐Otín et al., Cell, 153, 2013 and 1194). Human aging is associated with loss in skeletal muscle mass and function (Sarcopenia), contributing significantly to morbidity and mortality. Muscle aging is associated with loss of mtDNA integrity. In humans, clonally expanded mtDNA deletions colocalize with sites of fiber breakage and atrophy in skeletal muscle. mtDNA deletions may therefore play an important, possibly causal role in sarcopenia. The nematode Caenorhabditis elegans also exhibits age‐dependent decline in mitochondrial function and a form of sarcopenia. However, it is unclear if mtDNA deletions play a role in C. elegans aging. Here, we report identification of 266 novel mtDNA deletions in aging nematodes. Analysis of the mtDNA mutation spectrum and quantification of mutation burden indicates that (a) mtDNA deletions in nematode are extremely rare, (b) there is no significant age‐dependent increase in mtDNA deletions, and (c) there is little evidence for clonal expansion driving mtDNA deletion dynamics. Thus, mtDNA deletions are unlikely to drive the age‐dependent functional decline commonly observed in C. elegans. Computational modeling of mtDNA dynamics in C. elegans indicates that the lifespan of short‐lived animals such as C. elegans is likely too short to allow for significant clonal expansion of mtDNA deletions. Together, these findings suggest that clonal expansion of mtDNA deletions is likely a private mechanism of aging predominantly relevant in long‐lived animals such as humans and rhesus monkey and possibly in rodents.

Inter-individual differences in contamination profiles as tracer of social group association in stranded sperm whales

Ecological and physiological factors lead to different contamination patterns in individual marine mammals. The objective of the present study was to assess whether variations in contamination profiles are indicative of social structures of young male sperm whales as they might reflect a variation in feeding preferences and/or in utilized feeding grounds. We used a total of 61 variables associated with organic compounds and trace element concentrations measured in muscle, liver, kidney and blubber gained from 24 sperm whales that stranded in the North Sea in January and February 2016. Combining contaminant and genetic data, there is evidence for at least two cohorts with different origin among these stranded sperm whales; one from the Canary Island region and one from the northern part of the Atlantic. While genetic data unravel relatedness and kinship, contamination data integrate over areas, where animals occured during their lifetime. Especially in long-lived animals with a large migratory potential, as sperm whales, contamination data may carry highly relevant information about aggregation through time and space.