Disposable Soma Research Articles

No evidence of early life resource pulse effects on age-specific variation in survival, reproduction and body mass of female Siberian flying squirrels.

Understanding the diversity and causes of senescence patterns in the wild remains a challenging task, in particular among fast-living species for which senescence patterns have been poorly studied. Early life environmental conditions can shape senescence by influencing trade-offs between early and late life performance (disposable soma theory) or individual fitness through lifelong positive effects (silver spoon effects). Using a 23-year-long monitoring dataset of two populations of Siberian flying squirrels (Pteromys volans L.) in western Finland, we analysed the occurrence, onset and rate of senescence in female survival, body mass and reproductive performance. We also examined how early life pulsed resources (tree masting during the year of birth) influence age-specific variations in these traits. Our results indicate that survival senescence occurs after sexual maturity from 3 years of age. Females experiencing high resource availability at birth tended to survive better, but the age-specific trend was not affected by early life resource conditions. Maternal body mass declined slightly with age, starting at 4 years, regardless of early resource conditions. Similarly, among reproductive traits, we showed late-onset senescence in both litter size and annual reproductive probability, with no evidence supporting an effect of early life resources on these trends. We found no decline in juvenile body mass or in the juvenile size-number trade-off with maternal age. Our findings suggest that pulsed resources experienced at birth have a limited long-lasting impact on the life-history traits of this fast-living rodent, with no significant effect on senescence patterns.

Reproduction has immediate effects on female mortality, but no discernible lasting physiological impacts: A test of the disposable soma theory

The disposable soma theory (DST) posits that organisms age and die because of a direct trade-off in resource allocation between reproduction and somatic maintenance. DST predicts that investments in reproduction accentuate somatic damage which increase senescence and shortens lifespan. Here, we directly tested DST predictions in breeding and nonbreeding female C57BL/6J mice. We measured reproductive outputs, body composition, daily energy expenditure, and oxidative stress at peak lactation and over lifetime. We found that reproduction had an immediate and negative effect on survival due to problems encountered during parturition for some females. However, there was no statistically significant residual effect on survival once breeding had ceased, indicating no trade-off with somatic maintenance. Instead, higher mortality appeared to be a direct consequence of reproduction without long-term physiological consequences. Reproduction did not elevate oxidative stress. Our findings do not provide support for the predictions of the DST.

Agelessness is possible under the disposable soma theory but system complexity makes it unlikely

Although demographic studies have failed to find evidence of aging in certain animal species, classic evolutionary theories of aging struggle to explain how evolution could favor agelessness in such cases. Here, we develop mathematical models of the disposable soma theory to identify conditions in which agelessness would be evolutionarily favored. For any given type of damage that could accumulate and cause age-accelerating mortality risk, we find that evolution could select for its complete removal if the mortality risk it poses is severe enough and its repair does not pose too large of a penalty to reproduction. Environmental factors such as extrinsic mortality and the form of population density-dependent regulation also play a large role in determining the optimal rate of aging and whether agelessness should be evolutionarily favored. However, in a system with multiple sources of damage and multiple independent repair processes, avoiding aging is rarely evolutionarily favorable. Pleiotropic repair processes, such as those that could be present in asexual fissioning organisms, make agelessness more likely but do not guarantee it. Our results indicate that agelessness could be favored by evolution in narrow contexts but that multiple types of damage and repair make agelessness unlikely to arise in sufficiently complex organisms.

Understanding the Multifaceted Process of Aging: Theories, Mechanisms, and Implications for Treatment

The aging process is a multifaceted biological phenomenon characterized by alterations at the molecular, cellular, and organ levels that culminate in a gradual, unavoidable, and unavoidable reduction in the body's capacity to react suitably to internal and/or external stimuli. Aging is a complex process that involves different mechanisms as The "Wear and Tear" Theory ,The Genetic Control Theory ,The Neuroendocrine Theory ,Waste Accumulation Theory ,Divisions Theory, Autoimmune Theory, Thymic-Stimulating Theory ,Mitochondrial Theory Mitochondria, Errors and Repairs Theory, Redundant DNA Theory Cross-Linkage Theory , Death Hormone Theory (DECO), Caloric Restriction Theory ,The Rate of Living Theory ,Gene Mutation Theory, Accumulated mutations Theory, Theory, Order to Disorder Theory, Disposable soma Theory, Antagonistic pleiotropy theory, The Telomerase Theory ,The free radical Theory. The two main categories of aging theories that explain cellular aging are structural damage and programmed theories. Different types of cells experience physiological stressors due to a range of circumstances. Notably, post-mitotic and mitotic cells have different capacities for proliferation and age differently in response to these pressures through different processes of cellular senescence and death, respectively. Over time, these aging cells build up and eventually cause old tissues to malfunction. The aim of this review is to throw light upon the effected of aging and who to treatment it.

A unified framework for evolutionary genetic and physiological theories of aging.

Why and how we age are 2 intertwined questions that have fascinated scientists for many decades. However, attempts to answer these questions remain compartmentalized, preventing a comprehensive understanding of the aging process. We argue that the current lack of knowledge about the evolution of aging mechanisms is due to a lack of clarity regarding evolutionary theories of aging that explicitly involve physiological processes: the disposable soma theory (DST) and the developmental theory of aging (DTA). In this Essay, we propose a new hierarchical model linking genes to vital rates, enabling us to critically reevaluate the DST and DTA in terms of their relationship to evolutionary genetic theories of aging (mutation accumulation (MA) and antagonistic pleiotropy (AP)). We also demonstrate how these 2 theories can be incorporated in a unified hierarchical framework. The new framework will help to generate testable hypotheses of how the hallmarks of aging are shaped by natural selection.

Growth and longevity modulation through larval environment mediate immunosenescence and immune strategy of Tenebrio molitor

BackgroundThe Disposable Soma Theory of aging suggests a trade-off between energy allocation for growth, reproduction and somatic maintenance, including immunity. While trade-offs between reproduction and immunity are well documented, those involving growth remain under-explored. Rapid growth might deplete resources, reducing investment in maintenance, potentially leading to earlier or faster senescence and a shorter lifespan. However, rapid growth could limit exposure to parasitism before reaching adulthood, decreasing immunity needs. The insect immunity’s components (cellular, enzymatic, and antibacterial) vary in cost, effectiveness, and duration. Despite overall immunity decline (immunosenescence), its components seem to age differently. We hypothesize that investment in these immune components is adjusted based on the resource cost of growth, longevity, and the associated risk of parasitism.ResultsWe tested this hypothesis using the mealworm beetle, Tenebrio molitor as our experimental subject. By manipulating the larval environment, including three different temperatures and three relative humidity levels, we achieved a wide range of growth durations and longevities. Our main focus was on the relationship between growth duration, longevity, and specific immune components: hemocyte count, phenoloxidase activity, and antibacterial activity. We measured these immune parameters both before and after exposing the individuals to a standard bacterial immune challenge, enabling us to assess immune responses. These measurements were taken in both young and older adult beetles. Upon altering growth duration and longevity by modifying larval temperature, we observed a more pronounced investment in cellular and antibacterial defenses among individuals with slow growth and extended lifespans. Intriguingly, slower-growing and long-lived beetles exhibited reduced enzymatic activity. Similar results were found when manipulating larval growth duration and adult longevity through variations in relative humidity, with a particular focus on antibacterial activity.ConclusionThe impact of growth manipulation on immune senescence varies by the specific immune parameter under consideration. Yet, in slow-growing T. molitor, a clear decline in cellular and antibacterial immune responses with age was observed. This decline can be linked to their initially stronger immune response in early life. Furthermore, our study suggests an immune strategy favoring enhanced antibacterial activity among slow-growing and long-lived T. molitor individuals.

Expanding evolutionary theories of ageing to better account for symbioses and interactions throughout the Web of Life.

How, when, and why organisms age are fascinating issues that can only be fully addressed by adopting an evolutionary perspective. Consistently, the main evolutionary theories of ageing, namely the Mutation Accumulation theory, the Antagonistic Pleiotropy theory, and the Disposable Soma theory, have formulated stimulating hypotheses that structure current debates on both the proximal and ultimate causes of organismal ageing. However, all these theories leave a common area of biology relatively under-explored. The Mutation Accumulation theory and the Antagonistic Pleiotropy theory were developed under the traditional framework of population genetics, and therefore are logically centred on the ageing of individuals within a population. The Disposable Soma theory, based on principles of optimising physiology, mainly explains ageing within a species. Consequently, current leading evolutionary theories of ageing do not explicitly model the countless interspecific and ecological interactions, such as symbioses and host-microbiomes associations, increasingly recognized to shape organismal evolution across the Web of Life. Moreover, the development of network modelling supporting a deeper understanding on the molecular interactions associated with ageing within and between organisms is also bringing forward new questions regarding how and why molecular pathways associated with ageing evolved. Here, we take an evolutionary perspective to examine the effects of organismal interactions on ageing across different levels of biological organisation, and consider the impact of surrounding and nested systems on organismal ageing. We also apply this perspective to suggest open issues with potential to expand the standard evolutionary theories of ageing.

Dog Life Spans and the Evolution of Aging.

AbstractThe basic tenets of the evolutionary theories of senescence are well supported. However, there has been little progress in determining the relative influences of mutation accumulation and life history optimization. The causes of the well-established inverse relationship between life span and body size across dog breeds are used here to test these two classes of theories. The life span-body size relationship is confirmed for the first time after controlling for breed phylogeny. The life span-body size relationship cannot be explained by evolutionary responses to differences in extrinsic mortality either of contemporary breeds or of breeds at their establishment. The development of breeds larger and smaller than ancestral gray wolves has occurred through changes in early growth rate. This may explain the increase in the minimum age-dependent mortality rate with breed body size and thus higher age-dependent mortality throughout adult life. The main cause of this mortality is cancer. These patterns are consistent with the optimization of life history as described by the disposable soma theory of the evolution of aging. The dog breed life span-body size relationship may be the result of the evolution of greater defense against cancer lagging behind the rapid increase in body size during recent breed establishment.

The Effects of Graded Levels of Calorie Restriction: XIX. Impact of Graded Calorie Restriction on Protein Expression in theLiver.

Calorie restriction (CR) extends life span by modulating the mechanisms involved in aging. We quantified the hepatic proteome of male C57BL/6 mice exposed to graded levels of CR (0%-40% CR) for 3months, and evaluated which signaling pathways were most affected. The metabolic pathways most significantly stimulated by the increase in CR, included the glycolysis/gluconeogenesis pathway, the pentose phosphate pathway, the fatty acid degradation pathway, the valine, leucine, and isoleucine degradation pathway, and the lysine degradation pathway. The metabolism of xenobiotics by cytochrome P450 pathway was activated and feminized by increased CR, while production in major urinary proteins (Mups) was strongly reduced, consistent with a reduced investment in reproduction as predicted by the disposable soma hypothesis. However, we found no evidence of increased somatic protection, and none of the 4 main pathways implied to be linked to the impact of CR on life span (insulin/insulin-like growth factor [IGF-1], nuclear factor-κB [NF-κB], mammalian Target of Rapamycin [mTOR], and sirtuins) as well as pathways in cancer, were significantly changed at the protein level in relation to the increase in CR level. This was despite previous work at the transcriptome level in the same individuals indicating such changes. On the other hand, we found Aldh2, Aldh3a2, and Aldh9a1 in carnitine biosynthesis and Acsl5 in carnitine shuttle system were up-regulated by increased CR, which are consistent with our previous work on metabolome of the same individuals. Overall, the patterns of protein expression were more consistent with a "clean cupboards" than a "disposable soma" interpretation.

CeLab, a microfluidic platform for the study of life history traits, reveals metformin and SGK-1 regulation of longevity and reproductive span.

The potential to carry out high-throughput assays in a whole organism in a small space is one of the benefits of C. elegans, but worm assays often require a large sample size with frequent physical manipulations, rendering them highly labor-intensive. Microfluidic assays have been designed with specific questions in mind, such as analysis of behavior, embryonic development, lifespan, and motility. While these devices have many advantages, current technologies to automate worm experiments have several limitations that prevent widespread adoption, and most do not allow analyses of reproduction-linked traits. We developed a miniature C. elegans lab-on-a-chip device, CeLab, a reusable, multi-layer device with 200 separate incubation arenas that allows progeny removal, to automate a variety of worm assays on both individual and population levels. CeLab enables high-throughput simultaneous analysis of lifespan, reproductive span, and progeny production, refuting assumptions about the disposable soma hypothesis. Because CeLab chambers require small volumes, the chip is ideal for drug screens; we found that drugs previously shown to increase lifespan also increase reproductive span, and we discovered that low-dose metformin increases both. CeLab reduces the limitations of escaping and matricide that typically limit plate assays, revealing that feeding with heat-killed bacteria greatly extends lifespan and reproductive span of mated animals. CeLab allows tracking of life history traits of individuals, which revealed that the nutrient-sensing mTOR pathway mutant, sgk-1, reproduces nearly until its death. These findings would not have been possible to make in standard plate assays, in low-throughput assays, or in normal population assays.

Modalities of aging in organisms with different strategies of resource allocation.

Although the progress of aging research relies heavily on a theoretical framework, today there is no consensus on many critical questions in aging biology. I hypothesize that a systematic analysis of the intersection of different evolutionary mechanisms of aging with diverse resource allocation strategies in different organisms may reconcile aging hypotheses. The application of disposable soma, mutation accumulation, antagonistic pleiotropy, and life-history theory is considered across organisms with asexual reproduction, organisms with sexual reproduction and indeterminate growth in different conditions of extrinsic mortality, and organisms with determinate growth, with endotherms/homeotherms as a subgroup. This review demonstrates that different aging mechanisms are complementary to each other, and in organisms with different resource allocation strategies they form aging modalities ranging from immortality to suicidal programs. It also revamps the role of growth arrest in aging. Growth arrest evolved in many different groups of organisms as a result of resource reallocation from growth to reproduction (e.g., semelparous animals, holometabolic insects), or from growth to nutrient storage (endotherms/homeotherms). Growth arrest in different animal lineages has similar molecular mechanisms and similar consequences for longevity due to the conflict between growth-promoting and growth-suppressing programs and suppression of regenerative capacity.

“Born with a silver spoon in the mouth has bad sides too”: Experimentally increasing growth rate enhances individual quality but accelerates reproductive senescence in females of the mealworm beetle, Tenebrio molitor

Senescence occurs because of the decline of the strength of selection with age, allowing late-life reduced performances not being counter selected. From there, several phenomena may explain late-life reduced performances, such as the accumulation of deleterious mutations, the expression of pleiotropic genes or the existence of resource trade-offs between early and late performances. This latter phenomenon is at the core of the disposable soma theory of aging, which predicts that growth and early-life reproduction have costs that increase reproductive and actuarial senescence. Whereas the impact of the cost of early reproduction on reproductive and actuarial senescence has been extensively studied, that of the cost of growth remains overlooked and often inconclusive, possibly because of confounding effects associated with the procedures used to manipulate growth rate. Here, we investigated the cost of growth rate and its impact on reproductive senescence and longevity of females of the mealworm beetle, Tenebrio molitor. For this purpose, we generated insects with contrasted growth rates by raising groups of them in conditions below, above and optimal relative humidity (RH: 55, 85 and 70%, respectively) during the larval stage. The resulting adult females then bred, under the same optimal RH conditions, early in life, then later in life and were followed there until death. We found that larvae grown under the highest relative humidity exhibited the highest larval growth rate, thanks to both shorter growth duration and the achievement of heavier pupae mass. Adult females from this favorable growing condition lived longer, were more fecund early in life, but suffered from lower late-life reproductive investment. Our study shows that growth rate, which is highly dependent on the early-life environment, is an important factor modulating adult reproductive senescence, through the occurrence of early-late life trade-offs.

The damage-independent evolution of ageing by selective destruction

Ageing is widely believed to reflect the accumulation of molecular damage due to energetic costs of maintenance, as proposed in disposable soma theory (DST). Here we use agent-based modelling to describe an alternative theory by which ageing could undergo positive selection independent of energetic costs. We suggest that the selective advantage of aberrant cells with fast growth might necessitate a mechanism of counterselection we name selective destruction that specifically removes the faster cells from tissues, preventing the morbidity and mortality risks they pose. The resulting survival advantage of slower mutants could switch the direction of selection, allowing them to outcompete both fast mutants and wildtype cells, causing them to spread and induce ageing in the form of a metabolic slowdown. Selective destruction could therefore provide a proximal cause of ageing that is both consistent with the gene expression hallmarks of ageing, and independent of accumulating damage. Furthermore, negligible senescence would acquire a new meaning of increased basal mortality.

Large and expensive brain comes with a short lifespan: The relationship between brain size and longevity among fish taxa.

Vertebrates show substantial interspecific variation in brain size in relation to body mass. It has long been recognized that the evolution of large brains is associated with both costs and benefits, and it is their net benefit which should be favoured by natural selection. On one hand, the substantial energetic cost imposed by the maintenance of neural tissue is expected to compromise the energetic budget of organisms with large brains and their investment in other critical organs (expensive brain framework, EBF) or important physiological process, such as somatic maintenance and repair, thus accelerating ageing that shortens lifespan, as predicted by the disposable soma theory (DST). However, selection towards larger brain size can provide cognitive benefits (e.g., high behavioural flexibility) that may mitigate extrinsic mortality pressures, and thus may indirectly select for slower ageing that prolongs lifespan, as predicted by the cognitive buffer hypothesis (CBH). The relationship between longevity and brain size has been investigated to date only among terrestrial vertebrates, although the same selective forces acting on those species may also affect vertebrates living in aquatic habitats, such as fish. Thus, whether this evolutionary trade‐off for brain size and longevity exists on a large scale among fish clades remains to be addressed. In this study, using a global dataset of 407 fish species, I undertook the first phylogenetic test of the brain size/longevity relationship in aquatic vertebrate species. The study revealed a negative relationship between brain size and longevity among cartilaginous fish confirming EBF and DST. However, no pattern emerged among bony fish species. Among sharks and rays, the high metabolic cost of producing neural tissue transcends the cognitive benefits of evolving a larger brain. Consequently, my findings suggest that the cost of maintaining brain tissue is relatively higher in ectothermic species than in endothermic ones.

Reproductive effort and terminal investment in a multispecies assemblage of Amazon electric fish

AbstractThe terminal investment hypothesis (TIH) predicts that individuals with favorable prospects for future reproduction (i.e., high residual reproductive value, RRV) should moderate current reproductive investment in favor of growth, survival, and future reproduction, whereas those with low RRV should “terminally invest” by diverting somatic resources towards current reproduction at the expense of future reproduction. However, support for the TIH in wild animal populations is fragmentary, and the ecological contexts of terminal investment remain poorly known. We report a remarkable case of simultaneous terminal investment involving five sympatric species of the electric knifefish genus Brachyhypopomus, from Amazonian floodplain and terra firme stream habitats. We found that terminal investment is synchronized by seasonal breeding, in response to circannual environmental variation in mortality risk. Four species exhibit a uniseasonal iteroparous (annual) life history with complete post‐reproductive mortality after a single breeding season. One species (Brachyhypopomus beebei) exhibits a 2‐year multiseasonal iteroparous life history with breeding in two seasons and post‐reproductive mortality after the second. In mature females and (most) males of the annual species, as well as in both mature female and male second‐year (but not first‐year) B. beebei, we documented an increase in two metrics of reproductive effort (size‐adjusted gonad mass and electric signal amplitude) and a concomitant reduction in somatic condition (size‐adjusted somatic mass), all in response to proximity to the end of the common breeding season, when RRV approximates zero. In mature first‐year B. beebei, we documented neither an increase in reproductive effort nor a decline in somatic condition, implying an alternative strategy of reproductive restraint. Our findings support Kirkwood's disposable soma theory, which posits that death by reproductive exhaustion can be delayed if terminal investment is replaced by reproductive restraint, allowing individuals to survive and breed in a subsequent season. Deferral of the terminal investment response in annual species, and the origin of a gonadal regression‐regeneration sequence, may open pathways for rapid evolutionary transitions to multiseasonal iteroparity. Excepting the age (year‐group) dependency of terminal investment in B. beebei, we were unable to identify intrinsic cues or extrinsic environmental cues for the terminal investment response in Brachyhypopomus.

Determine the constraints on the evolution of replicative aging in changing environment

Many fundamental questions regarding aging and its underlying mechanisms remain elusive. In particular, the answer to the most basic question—why do we age at all?—is still not fully understood. Some theories suggest that aging is the result of fundamental limitations on natural selection. These include mutations with late-age deleterious effects (mutation accumulation), selection of genes that are beneficial early in life but are deleterious at late-age (antagonistic pleiotropy ) and the existence of a tradeoff between damage repair and reproduction (disposable soma).

Telomeres, aging, and cancer: the big picture

AbstractThe role of telomeres in human health and disease is yet to be fully understood. The limitations of mouse models for the study of human telomere biology and difficulties in accurately measuring the length of telomere repeats in chromosomes and cells have diverted attention from many important and relevant observations. The goal of this perspective is to summarize some of these observations and to discuss the antagonistic role of telomere loss in aging and cancer in the context of developmental biology, cell turnover, and evolution. It is proposed that both damage to DNA and replicative loss of telomeric DNA contribute to aging in humans, with the differences in leukocyte telomere length between humans being linked to the risk of developing specific diseases. These ideas are captured in the Telomere Erosion in Disposable Soma theory of aging proposed herein.

The effects of graded calorie restriction XVII: Multitissue metabolomics reveals synthesis of carnitine and NAD, and tRNA charging as key pathways

The evolutionary context of why caloric restriction (CR) activates physiological mechanisms that slow the process of aging remains unclear. The main goal of this analysis was to identify, using metabolomics, the common pathways that are modulated across multiple tissues (brown adipose tissue, liver, plasma, and brain) to evaluate two alternative evolutionary models: the "disposable soma" and "clean cupboards" ideas. Across the four tissues, we identified more than 10,000 different metabolic features. CR altered the metabolome in a graded fashion. More restriction led to more changes. Most changes, however, were tissue specific, and in some cases, metabolites changed in opposite directions in different tissues. Only 38 common metabolic features responded to restriction in the same way across all four tissues. Fifty percent of the common altered metabolites were carboxylic acids and derivatives, as well as lipids and lipid-like molecules. The top five modulated canonical pathways were l-carnitine biosynthesis, NAD (nicotinamide adenine dinucleotide) biosynthesis from 2-amino-3-carboxymuconate semialdehyde, S-methyl-5'-thioadenosine degradation II, NAD biosynthesis II (from tryptophan), and transfer RNA (tRNA) charging. Although some pathways were modulated in common across tissues, none of these reflected somatic protection, and each tissue invoked its own idiosyncratic modulation of pathways to cope with the reduction in incoming energy. Consequently, this study provides greater support for the clean cupboards hypothesis than the disposable soma interpretation.

The soma-germline communication: implications for somatic and reproductive aging

Aging is characterized by a functional decline in most physiological processes, including alterations in cellular metabolism and defense mechanisms. Increasing evidence suggests that caloric restriction extends longevity and retards age-related diseases at least in part by reducing metabolic rate and oxidative stress in a variety of species, including yeast, worms, flies, and mice. Moreover, recent studies in invertebrates – worms and flies, highlight the intricate interrelation between reproductive longevity and somatic aging (known as disposable soma theory of aging), which appears to be conserved in vertebrates. This review is specifically focused on how the reproductive system modulates somatic aging and vice versa in genetic model systems. Since many signaling pathways governing the aging process are evolutionarily conserved, similar mechanisms may be involved in controlling soma and reproductive aging in vertebrates.

Positive early-late life-history trait correlations in elephant seals.

Correlations between early- and late-life performance are a major prediction of life-history theory. Negative early-late correlations can emerge because biological processes are optimized for early but not late life (e.g., rapid development may accelerate the onset of senescence; "developmental theory of aging") or because allocation to early-life performance comes at a cost in terms of late-life performance (as in the disposable soma theory). But variation in genetic and environmental challenges that each individual has to cope with during early life may also lead to positive early-late life-history trait correlations (the "fixed heterogeneity" or "individual quality" hypothesis). We analyzed individual life-history trajectories of 7,420 known-age female southern elephant seals (Mirounga leonina) monitored over 36yr to determine how actuarial senescence (a proxy for late-life performance) correlate with age at first reproduction (a proxy for early-life performance). As some breeding events may not be detected in this field study, we used a custom "multievent" hierarchical model to estimate the age at first reproduction and correlate it to other life-history traits. The probability of first reproduction was 0.34 at age 3, with most females breeding for the first time at age 4, and comparatively few at older ages. Females with an early age of first reproduction outperformed delayed breeders in all aspects we considered (survival, rate of senescence, net reproductive output) but one: early breeders appeared to have an onset of actuarial senescence 1 yr earlier compared to late breeders. Genetics and environmental conditions during early life likely explain the positive correlation between early- and late-life performance. Our results provide the first evidence of actuarial senescence in female southern elephant seals.