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Parental age at offspring conception often influences offspring longevity, but the mechanisms underlying this link are poorly understood. One mechanism that may be important is telomeres, highly conserved, repetitive sections of non‐coding DNA that form protective caps at chromosome ends and are often positively associated with longevity. Here, the potential pathways by which the age of the parents at the time of conception may impact offspring telomeres are described first, including direct effects on parental gamete telomeres and indirect effects on offspring telomere loss during pre‐ or post‐natal development. Then a surge of recent studies demonstrating the effects of parental age on offspring telomeres in diverse taxa are reviewed. In doing so, important areas for future research and experimental approaches that will enhance the understanding of how and when these effects likely occur are highlighted. It is concluded by considering the potential evolutionary consequences of parental age on offspring telomeres.

 

Decades of research into stress responses have highlighted large variation among individuals, populations, and species, and the sources of this variation have been a center of research across disciplines. The most common measure of the vertebrate stress response is glucocorticoids. However, the predictive power of glucocorticoid responses to fitness is surprisingly low. This is partly because the hormone levels rapidly change in response to stressor exposure and elevated levels at one time point can indicate either that glucocorticoids are helping the organism cope with the stressor or that dysregulation of hormone release is harming the organism. Meaning, the fitness consequences of the stressor depends on how efficient the stress responses are at negating the harmful impacts of stressors to cells and tissues. To encompass the idea of the efficiency of stress responses and to integrate cellular and organismal stress responses, a new theoretical model called the Damage-Fitness Model was developed. The model focuses on the downstream effects of stress responses and predicts that the accumulation of damage in cells and tissues (e.g., persistent damage to proteins, lipids, and DNA) negatively impacts fitness components. In this mini-review, we examine evidence supporting the Damage-Fitness Model and explore new directions forward.

 

Although most organisms respond to environmental and social stressors by initiating a stress response that is expected to increase fitness, we currently lack information about how the stress response is integrated across levels of biological organization. Organismal biologists and physiological ecologists have tended to focus on questions related to how the glucocorticoid stress response varies across ecological contexts and is related to fitness, whereas, molecular and cellular biologists have typically investigated the fundamental underlying mechanisms. However, it is becoming increasingly clear that a comprehensive understanding of the evolution of the stress response will require integrative studies that span levels of analyses. This information will be critical for predicting how selection will influence the expression of this complex phenotype at the organismal level, as well as how the integration of the underlying mechanisms will influence the evolutionary response to selection. As diverse organisms are expected to experience rising stress exposure in the face of anthropogenic disturbance and climate change, this information is becoming increasingly urgent. The overarching goals of this symposium were to bring together researchers that study the stress response across levels of organization in diverse organisms to identify important gaps in knowledge and novel research approaches that could be used to advance the field.

 

Annual reproductive success is often highest in individuals that initiate breeding early, yet relatively few individuals start breeding during this apparently optimal time. This suggests that individuals, particularly females who ultimately dictate when offspring are born, incur costs by initiating reproduction early in the season. We hypothesized that increases in the ageing rate of somatic cells may be one such cost. Telomeres, the repetitive DNA sequences on the ends of chromosomes, may be good proxies of biological wear and tear as they shorten with age and in response to stress. Using historical data from a long‐term study population of dark‐eyed juncos (Junco hyemalis), we found that telomere loss between years was greater in earlier breeding females, regardless of chronological age. There was no relationship between telomere loss and the annual number of eggs laid or chicks that reached independence. However, telomere loss was greater when temperatures were cooler, and cooler temperatures generally occur early in the season. This suggests that environmental conditions could be the primary cause of accelerated telomere loss in early breeders.

 

Abstract Although the pace of senescence varies considerably, the physiological systems that contribute to different patterns of senescence are not well understood, especially in long-lived vertebrates. Long-lived bony fish (i.e., Class Osteichthyes) are a particularly useful model for studies of senescence because they can readily be aged and exhibit some of the longest lifespans among vertebrates. In this study we examined the potential relationship between age and multiple physiological systems including: stress levels, immune function, and telomere length in individuals ranging in age from 2 to 99 years old in bigmouth buffalo ( Ictiobus cyprinellus ), the oldest known freshwater teleost fish. Contrary to expectation, we did not find any evidence for age-related declines in these physiological systems. Instead, older fish appeared to be less stressed and had greater immunity than younger fish, suggesting age-related improvements rather than declines in these systems. There was no significant effect of age on telomeres, but individuals that may be more stressed had shorter telomeres. Taken together, these findings suggest that bigmouth buffalo exhibit negligible senescence in multiple physiological systems despite living for nearly a century. 

The mechanisms that contribute to variation in lifetime reproductive success are not well understood. One possibility is that telomeres, conserved DNA sequences at chromosome ends that often shorten with age and stress exposures, may reflect differences in vital processes or influence fitness. Telomere length often predicts longevity, but longevity is only one component of fitness and little is known about how lifetime reproductive success is related to telomere dynamics in wild populations. We examined the relationships between telomere length beginning in early life, telomere loss into adulthood and lifetime reproductive success in free-living house sparrows ( Passer domesticus ). We found that females, but not males, with longer telomeres during early life had higher lifetime reproductive success, owing to associations with longevity and not reproduction per year or attempt. Telomeres decreased with age in both sexes, but telomere loss was not associated with lifetime reproductive success. In this species, telomeres may reflect differences in quality or condition rather than the pace of life, but only in females. Sexually discordant selection on telomeres is expected to influence the stability and maintenance of within population variation in telomere dynamics and suggests that any role telomeres play in mediating life-history trade-offs may be sex specific. 

Parental age can affect offspring telomere length through heritable and epigenetic-like effects, but at what stage during development these effects are established is not well known. To address this, we conducted a cross-fostering experiment in common gulls (Larus canus) that enabled us distinguish between pre-and post-natal parental age effects on offspring telomere length. Whole clutches were exchanged after clutch completion within and between parental age classes (young and old) and blood samples were collected from chicks at hatching and during the fastest growth phase (11 days later) to measure telomeres. Neither the ages of the natal nor the foster parents predicted the telomere length or the change in telomere lengths of their chicks. Telomere length (TL) was repeatable within chicks, but increased across development (repeatability = 0.55, intraclass correlation coefficient within sampling events 0.934). Telomere length and the change in telomere length were not predicted by post-natal growth rate. Taken together, these findings suggest that in common gulls, telomere length during early life is not influenced by parental age or growth rate, which may indicate that protective mechanisms buffer telomeres from external conditions during development in this relatively long-lived species.