Covariation between glucocorticoid levels and receptor expression modulates embryo development and postnatal phenotypes in gulls.

The hypothalamic-pituitary-adrenocortical axis can translate, through glucocorticoid secretion, the prenatal environment to development to produce phenotypes that match prevailing environmental conditions. However, whether developmental plasticity is modulated by the interaction between circulating glucocorticoids and receptor expression remains unclear. Here, we tested whether covariation between plasma corticosterone (CORT) and glucocorticoid receptor gene (Nr3c1) expression in blood underlies embryonic developmental programming in yellow-legged gulls (Larus michahellis). We examined variations in circulating levels of CORT and the expression and DNA methylation patterns of Nr3c1 in response to two ecologically relevant prenatal factors: adult alarm calls (a cue of predator presence) and changes in prenatal light environment (a cue of competitive disadvantage). We then determined whether embryonic development and postnatal phenotypes were associated with CORT levels and Nr3c1 expression, and explored direct and indirect relationships between the prenatal environment, hormone-receptor covariation, and postnatal phenotypes. Prenatal exposure to alarm calls increased CORT levels and up-regulated Nr3c1 expression in gull chicks, while exposure to light cues reduced both hormone levels and receptor expression. Chicks prenatally exposed to alarm calls showed altered DNA methylation profiles in the Nr3c1 regulatory region, but patterns varied throughout the breeding season and between years. Moreover, our results suggest a negative relationship between DNA methylation and expression in Nr3c1 , at least at specific CpG sites. The interplay between circulating CORT and Nr3c1 expression affected embryo developmental timing and vocalizations, as well as hatchling mass and fitness-relevant behaviours. These findings provide a link between prenatal inputs, glucocorticoid function and phenotypic outcomes, suggesting that hormone-receptor interaction may underlie developmental programming in free-living animals.

Maternal testosterone affects offspring telomerase activity in a long-lived seabird.

Androgens are a group of steroid hormones that have long been proposed as a mechanism underpinning intergenerational plasticity. In birds, maternally allocated egg testosterone, one of the main androgens in vertebrates, affects a wide variety of offspring phenotypic traits but the mechanisms underlying this form of intergenerational plasticity are not yet well understood. Recent in vitro and animal model studies have shown that telomerase expression and activity are important targets of androgen signaling. The telomerase enzyme is known for its repair function on telomeres, the DNA-protein complexes at the ends of chromosomes that are involved in genomic integrity and cell aging. However, the role of maternal testosterone in influencing offspring telomerase levels in natural populations and its consequences on telomere length and potentially on offspring development is still unknown. Here, by experimentally modifying the level of egg testosterone in a natural population of yellow-legged gull (Larus michahellis), we show that chicks hatched from testosterone-treated eggs had higher average levels of telomerase and faster growth than controls during the first week of life. While testosterone-treated chicks also tended to have longer telomeres than controls at hatching this difference disappeared by day 6 of age. Overall, our results suggest that maternal testosterone may have a potential adaptive value by promoting offspring growth and presumably telomerase levels, as this enzyme plays other important physiological functions (e.g., stress resistance, cell signaling, or tissue genesis) besides telomere lengthening. Nonetheless, our knowledge of the potential adaptive function of telomerase in natural populations is scarce and so the potential pathways linking maternal hormones, offspring telomerase, and fitness should be further investigated.

Telomerase activity can mediate the effects of growth on telomeres during post-natal development in a wild bird.

In wild animals, telomere attrition during early development has been linked with several fitness disadvantages throughout life. Telomerase enzyme can elongate telomeres, but it is generally assumed that its activity is suppressed in most somatic tissues upon birth. However, recent evidence suggests that this may not be the case for long-lived bird species. We have therefore investigated whether telomerase activity is maintained during the postnatal growth period in a wild yellow-legged gull (Larus michahellis) population. Our results indicate that telomerase activity is not negligible in the blood cells, but activity levels sharply decline from hatching to fledging following a similar pattern to the reduction observed in telomere length. Our results further suggest that the observed variation in telomere length may be the result of a negative effect of fast growth on telomerase activity, thus providing a new mechanism through which growth rates may affect telomere dynamics and potentially life-history trajectories.

Environment-induced changes in reproductive strategies and their transgenerational effects in the three-spined stickleback.

An organism may increase its fitness by changing its reproductive strategies in response to environmental cues, but the possible consequences of those changes for the next generation have rarely been explored. By using an experiment on the three-spined stickleback (Gasterosteus aculeatus), we studied how changes in the onset of breeding photoperiod (early versus late) affect reproductive strategies of males and females, and life histories of their offspring. We also explored whether telomeres are involved in the within- and transgenerational effects. In response to the late onset of breeding photoperiod, females reduced their investment in the early clutches, but males increased their investment in sexual signals. Costs of increased reproductive investment in terms of telomere loss were evident only in the late females. The environmentally induced changes in reproductive strategies affected offspring growth and survival. Most notably, offspring growth rate was the fastest when both parents experienced a delayed (i.e., late) breeding photoperiod, and survival rate was the highest when both parents experienced an advanced (i.e., early) breeding photoperiod. There was no evidence of transgenerational effects on offspring telomere length despite positive parents-offspring relationships in this trait. Our results highlight that environmental changes may impact more than one generation by altering reproductive strategies of seasonal breeders with consequences for offspring viability.

Gull chicks grow faster but lose telomeres when prenatal cues mismatch the real presence of sibling competitors.

During embryonic life, individuals should adjust their phenotype to the conditions that they will encounter after birth, including the social environment, if they have access to (social) cues that allow them to forecast future conditions. In birds, evidence indicates that embryos are sensitive to cues from clutch mates, but whether embryos adjust their development to cope with the expected level of sibling competition has not hitherto been investigated. To tackle this question, we performed a 'match versus mismatch' experimental design where we manipulated the presence of clutch mates (i.e. clutch size manipulation) and the real (postnatal) level of sibling competition (i.e. brood size manipulation) in the yellow-legged gull (Larus michahellis). We provide evidence that the prenatal cues of sibling presence induced developmental changes (such as epigenetic profiles) that had programming effects on chick begging behaviour and growth trajectories after hatching. While receiving mismatching information favoured chick begging and growth, this came at the cost of reduced antioxidant defences and a premature loss of telomeres. Our findings highlight the role of the prenatal social environment in developmental plasticity and suggest that telomere attrition may be an important physiological cost of phenotype-environment mismatch.

Reduced telomere length in embryos exposed to predator cues.

It is often assumed that embryos are isolated from external influences, but recent studies indicate that environmental stressors during prenatal stages can exert long-term negative effects on fitness. A potential mechanism by which predation risk may lastingly shape life-history traits and phenotypes is via effects on telomeres. However, whether prenatal exposure to environmental stressors, such as cues of predator presence, affects postnatal telomere length has not hitherto been investigated. Using an experimental design in which we modified the exposure of yellow-legged gull (Larus michahellis) embryos to social cues of predator presence (i.e. alarm calls), we show that prenatally exposed chicks had shorter telomeres after hatching. As young birds with shorter telomere lengths have reduced fledging success, reproductive success and lifespan, the reduced telomere length in the exposed chicks is likely to have long-term fitness consequences. Moreover, our results provide a mechanistic link through which predators may negatively affect population dynamics.

Bird embryos perceive vibratory cues of predation risk from clutch mates.

During development in fluctuating environments, phenotypes can be adjusted to the conditions that individuals will probably encounter later in life. As developing embryos have a limited capacity to fully capture environmental information, theory predicts that they should integrate relevant information from all reliable sources, including the social environment. In many oviparous species, embryos are able to perceive cues of predator presence in some circumstances, but whether this information is socially transmitted among clutch mates-promoting phenotypic adjustments in the whole clutch-is unknown. Here, using an experimental design for which we modified the exposure to some, but not all, embryos of the same clutch to cues of predator presence (that is, alarm calls), we show that exposed embryos of the yellow-legged gull (Larus michahellis) and their unexposed clutch mates showed similar developmental changes that were absent in embryos from control clutches. Compared with the control broods, both embryos that were exposed to alarm calls and their unexposed clutch mates showed altered prenatal and postnatal behaviours, higher levels of DNA methylation and stress hormones, and reduced growth and numbers of mitochondria (which may be indicative of the capacity for energy production of cells). These results strongly suggest that gull embryos are able to acquire relevant environmental information from their siblings. Together, our results highlight the importance of socially acquired information during the prenatal stage as a non-genetic mechanism promoting developmental plasticity.

Redox-regulation and life-history trade-offs: scavenging mitochondrial ROS improves growth in a wild bird.

It has been proposed that animals usually restrain their growth because fast growth leads to an increased production of mitochondrial reactive oxygen species (mtROS), which can damage mitochondrial DNA and promote mitochondrial dysfunction. Here, we explicitly test whether this occurs in a wild bird by supplementing chicks with a mitochondria-targeted ROS scavenger, mitoubiquinone (mitoQ), and examining growth rates and mtDNA damage. In the yellow-legged gull Larus michahellis, mitoQ supplementation increased the early growth rate of chicks but did not reduce mtDNA damage. The level of mtDNA damage was negatively correlated with chick mass, but this relationship was not affected by the mitoQ treatment. We also found that chick growth was positively correlated with both mtDNA copy number and the mitochondrial enzymatic activity of citrate synthase, suggesting a link between mitochondrial content and growth. Additionally, we found that MitoQ supplementation increased mitochondrial content (in males), altered the relationship between mtDNA copy number and damage, and downregulated some transcriptional pathways related to cell rejuvenation, suggesting that scavenging mtROS during development enhanced growth rates but at the expense of cellular turnover. Our study confirms the central role of mitochondria modulating life-history trade-offs during development by other mechanisms than mtROS-inflicted damage.

Crickets increase sexual signalling and sperm protection but live shorter in the presence of rivals.

The sociosexual environment animals experience through their life can shape the evolution of key life history traits, including longevity. Male-male competition, for instance, may influence the resources allocated to traits involved in male reproductive success. Here, I test whether lifelong exposure to a competitor male influences male investment in pre- and post-copulatory sexual traits (calling effort and sperm quality) and how this affected the oxidative status and longevity of male field crickets (Gryllus bimaculatus). As expected, the visual exposure to a mating competitor promoted a higher calling effort in the male crickets but resulted in a decline in the haemolymph antioxidant content. The haemolymph antioxidant content negatively covaried with the antioxidant content of the sperm but interestingly, only when the males were exposed to a competitor. This suggests that when mating competition is high, males may prioritize sperm antioxidant protection against somatic maintenance. Finally, I provide evidence that male-male competition imposes additional costs to reproduction, as males exposed to a mating competitor lost a significant proportion of body antioxidant defences and body mass over time and in long term, had a reduced lifespan. Overall, this study strongly suggests that intrasexual competition may impose additional oxidative costs during reproduction for males, with negative consequences on lifespan. Moreover, the results highlight the role of oxidative stress as a physiological mechanism underlying the trade-off between reproduction-longevity and through which sexual selection may contribute to the evolution of senescence patterns.

Carry-over effects of early thermal conditions on somatic and germline oxidative damages are mediated by compensatory growth in sticklebacks.

Most studies of climate change impacts focus on the effects of summer temperatures, which can immediately impact fitness of breeders, but winter temperatures are expected to have a greater impact on development and growth of animals with long-lasting consequences. Exposure to warmer temperatures can increase cellular oxidative damage in ectotherms. Yet, it is unknown whether thermal stress during early life has prolonged effects on oxidative status during adulthood. In an experiment using F1 fish originated from a wild three-spined stickleback population at the southern edge of its European distribution, we examined whether experimental thermal conditions experienced in winter had carry-over effects on oxidative status and telomere length, a marker of accumulated stress, in the soma and germline during adulthood. For this, oxidative DNA damage, enzymatic antioxidant activities and telomere length were measured three months after the termination of the temperature manipulation. In addition, we tested whether such delayed effects, if any, were due to individuals' compensatory growth after experiencing unfavourable growth conditions in winter. Warm acclimation during winter induced increased levels of oxidative DNA damage in muscle and sperm and increased enzymatic antioxidant defences in muscle during the breeding season. Telomere length of adult fish was not influenced by thermal conditions experienced during early life. Winter temperature manipulation influenced fish to alter the temporal pattern of growth trajectories across the juvenile and adult stages. Fish reared in warm winter conditions grew at a slower rate than the controls during the period of temperature manipulation then accelerated body mass gain to catch up during the breeding season. Faster somatic growth during the breeding season incurred a higher cost in terms of oxidative damage in the warm-treated individuals. For the first time, we experimentally show the long-lasting detrimental effects of thermal stress on and the positive link between catch-up growth and oxidative DNA damage in the soma and germline. Winter temperature increases due to climate change can reduce fertility and survival of fish by inducing catch-up growth. The detrimental effects of winter climate change may accumulate across generations through the pre-mutagenic DNA damage in the germline.

La mayoría de los estudios sobre los efectos del cambio climático se centran en los efectos de las temperaturas estivales, ya que estas pueden afectar de forma inmediata a la eficacia biológica de los individuos reproductores. No obstante, es esperable que las temperaturas invernales tengan un mayor impacto a largo plazo debido a sus efectos durante el desarrollo y el crecimiento temprano. Aunque la exposición a temperaturas más elevadas puede aumentar el daño oxidativo celular en ectotermos, todavía se desconoce si un estrés térmico durante el desarrollo temprano tiene efectos a largo plazo sobre el estado oxidativo en la edad adulta. En este experimento, en el que usamos la F1 procedente de una población de pez espinoso situada al borde sur de su distribución, examinamos los efectos a largo plazo de las condiciones térmicas invernales sobre los niveles de estrés oxidativo y longitud telomérica de la línea somática y germinal en la edad adulta. Además, evaluamos si tales efectos a largo plazo, si los hubo, se relacionaron con las tasa de crecimiento de los individuos. La aclimatación cálida durante el invierno indujo un aumento de los niveles de daño oxidativo en al ADN del músculo y los espermatozoides durante la estación reproductora, así como un aumento de las defensas antioxidantes enzimáticas en el músculo. La longitud telomérica adulta no se vio influenciada por las condiciones térmicas experimentadas durante el desarrollo temprano. La manipulación de la temperatura invernal alteró la trayectoria de crecimiento de los peces a lo largo de la fase juvenil y adulta. Los peces criados en condiciones invernales cálidas crecieron a un ritmo más lento que los controles durante el período de manipulación pero posteriormente mostraron una mayor tasa de crecimiento. Este crecimiento compensatorio se completó durante la temporada de reproducción. Este crecimiento compensatorio durante la temporada de reproducción tuvo un coste más elevado, en términos de daño oxidativo, en los individuos que experimentaron una condiciones invernales más cálidas. Por primera vez mostramos experimentalmente que el estrés termino temprano tiene efectos perjudiciales a largo plazo, y que existe una relación positiva entre la tasa de crecimiento compensatorio y los niveles de daño oxidativo en el ADN de las línea somática y germinal. El aumento de las temperaturas invernales debido al cambio climático podría reducir la fertilidad y la supervivencia de las poblaciones de peces al inducir cambios en las tasas de crecimiento. Además, los efectos perjudiciales del cambio climático invernal podrían ser trans-generacionales como consecuencia de la acumulación de daños pre-mutagénicos en el ADN de la línea germinal.

Glucocorticoids modulate gastrointestinal microbiome in a wild bird.

It has recently been hypothesized that stress exposure (e.g. via glucocorticoid secretion) may dysregulate the bacterial gut microbiome, a crucial 'organ' in animal health. However, whether stress exposure (e.g. via glucocorticoid secretion) affects the bacterial gut microbiome of natural populations is unknown. We have experimentally altered the basal glucocorticoid level (corticosterone implants) in a wild avian species, the yellow-legged gull Larus michahellis, to assess its effects on the gastrointestinal microbiota. Our results suggest underrepresentation of several microbial taxa in the corticosterone-implanted birds. Importantly, such reduction included potentially pathogenic avian bacteria (e.g. Mycoplasma and Microvirga) and also some commensal taxa that may be beneficial for birds (e.g. Firmicutes). Our findings clearly demonstrate a close link between microbiome communities and glucocorticoid levels in natural populations. Furthermore, they suggest a beneficial effect of stress in reducing the risk of infection that should be explored in future studies.

Experimental demonstration that offspring fathered by old males have shorter telomeres and reduced lifespans.

Offspring of older parents frequently show reduced longevity, but the mechanisms driving this so-called 'Lansing effect' are unknown. While inheritance of short telomeres from older parents could underlie this effect, studies to date in different species have found mixed results, reporting positive, negative or no association between parental age and offspring telomere length (TL). However, most of the existing evidence is from non-experimental studies in which it is difficult to exclude alternative explanations such as differential survival of parents with different telomere lengths. Here we provide evidence in the zebra finch that offspring from older parents have reduced lifespans. As a first step in disentangling possible causes, we used an experimental approach to examine whether or not we could detect pre-natal paternal effects on offspring TL. We found that zebra finch embryos fathered by old males have shorter telomeres than those produced by the same mothers but with younger fathers. Since variation in embryonic TL persists into post-natal life, and early life TL is predictive of longevity in this species, this experimental study demonstrates that a paternally driven pre-natal TL reduction could at least in part underlie the reduced lifespan of offspring from older parents.

Postnatal nutrition influences male attractiveness and promotes plasticity in male mating preferences.

Poor early-life nutrition could reduce adult reproductive success by negatively affecting traits linked to sexual attractiveness such as song complexity. If so, this might favor strategic mate choice, allowing males with less complex songs to tailor their mating tactics to maximize the reproductive benefits. However, this possibility has been ignored in theoretical and empirical studies. By manipulating the micronutrient content of the diet (e.g., low or high) during the postnatal period of male zebra finches, we show for the first time (1) that males reared on a poor (low) micronutrient diet had less complex songs as adults; (2) that these males, in contrast to the high micronutrient diet group, were more selective in their mating strategies, discriminating against those females most likely to reduce their clutch size when paired with males having less complex songs; and (3) that by following different mating strategies, males reared on the contrasting diets obtained similar reproductive benefits. These results suggest that early-life dietary conditions can induce multiple and long-lasting effects on male and female reproductive traits. Moreover, the results seem to reflect a previously unreported case of adaptive plasticity in mate choice in response to a nutritionally mediated reduction in sexual attractiveness.

Family-transmitted stress in a wild bird.

Recent data suggest that, in animals living in social groups, stress-induced changes in behavior have the potential to act as a source of information, so that stressed individuals could themselves act as stressful stimuli for other individuals with whom they interact repeatedly. Such form of cross-over of stress may be beneficial if it enhances adaptive responses to ecological stressors in the shared environment. However, whether stress can be transferred among individuals during early life in natural populations remains unknown. Here we tested the effect of living with stressed siblings in a gull species where, as in many vertebrates, family represents the basic social unit during development. By experimentally modifying the level of stress hormones (corticosterone) in brood mates, we demonstrate that the social transfer of stress level triggers similar stress responses (corticosterone secretion) in brood bystanders. Corticosterone-implanted chicks and their siblings were faster in responding to a potential predator attack than control chicks. In gulls, fast and coordinated reactions to predators may increase the chances of survival of the whole brood, suggesting a beneficial fitness value of cross-over of stress. However, our data also indicate that living with stressed brood mates early in life entails some long-term costs. Near independence, fledglings that grew up with stressed siblings showed reduced body size, high levels of oxidative damage in lipids and proteins, and a fragile juvenile plumage. Overall, our results indicate that stress cross-over occurs in animal populations and may have important fitness consequences.

Embryonic and postnatal telomere length decrease with ovulation order within clutches.

Telomere length (TL) in early life has been found to be predictive of subsequent lifespan. Factors such as parental TL, parental age and environmental conditions during development have been shown to contribute to the observed variation in TL among individuals. One factor that has not hitherto been considered is ovulation order, although it is well established that the last hatched/born offspring in a brood or litter often show relatively poor subsequent performance. We examined the within- and across-clutch effect of ovulation order on TL in embryos of zebra finches experiencing the same controlled incubation conditions (N = 151), and tested whether any such ovulation order effects remained detectable in adults (N = 122). Irrespective of clutch and egg size, TL in early-stage embryos (72 h incubation) markedly decreased with within-clutch ovulation order; the difference in TL of first and last-laid embryos was equivalent to the average within-individual telomere loss over the entire period of nestling and juvenile life. This ovulation-order effect occurred only within but not across clutches, and was still evident in adults. Given that TL in early life predicts lifespan, our results suggest that parental effects on telomere length could contribute to the known poor performance of later-ovulated family members.

Voluntary locomotor activity mitigates oxidative damage associated with isolation stress in the prairie vole (Microtus ochrogaster).

Organismal performance directly depends on an individual's ability to cope with a wide array of physiological challenges. For social animals, social isolation is a stressor that has been shown to increase oxidative stress. Another physiological challenge, routine locomotor activity, has been found to decrease oxidative stress levels. Because we currently do not have a good understanding of how diverse physiological systems like stress and locomotion interact to affect oxidative balance, we studied this interaction in the prairie vole (Microtus ochrogaster). Voles were either pair housed or isolated and within the isolation group, voles either had access to a moving wheel or a stationary wheel. We found that chronic periodic isolation caused increased levels of oxidative stress. However, within the vole group that was able to run voluntarily, longer durations of locomotor activity were associated with less oxidative stress. Our work suggests that individuals who demonstrate increased locomotor activity may be better able to cope with the social stressor of isolation.

Interactive effects of early and later nutritional conditions on the adult antioxidant defence system in zebra finches.

In vertebrates, antioxidant defences comprise a mixture of endogenously produced components and exogenously obtained antioxidants that are derived mostly from the diet. It has been suggested that early-life micronutritional conditions might influence the way in which the antioxidant defence system operates, which could enable individuals to adjust the activity of the endogenous and exogenous components in line with their expected intake of dietary antioxidants if the future environment resembles the past. We investigated this possibility by experimentally manipulating the micronutrient content of the diet during different periods of postnatal development in the zebra finch (Taeniopygia guttata). Birds that had a low micronutrient diet during the growth phase initially had a lower total antioxidant capacity (TAC) than those reared under a high micronutrient diet, but then showed a compensatory response, so that by the end of the growth phase, the TAC of the two groups was the same. Interestingly, we found an interactive effect of micronutrient intake early and late in development: only those birds that continued with the same dietary treatment (low or high) throughout development showed a significant increase in their TAC during the period of sexual maturation. A similar effect was also found in the level of enzymatic antioxidant defences (glutathione peroxidase; GPx). No significant effects were found in the level of oxidative damage in lipids [malondialdehyde (MDA) levels]. These findings demonstrate the importance of early and late developmental conditions in shaping multiple aspects of the antioxidant system. Furthermore, they suggest that young birds may adjust their antioxidant defences to enable them to 'thrive' on diets rich or poor in micronutrients later in life.

Sex-dependent effects of nutrition on telomere dynamics in zebra finches (Taeniopygia guttata).

At a cellular level, oxidative stress is known to increase telomere attrition, and hence cellular senescence and risk of disease. It has been proposed that dietary micronutrients play an important role in telomere protection due to their antioxidant properties. We experimentally manipulated dietary micronutrients during early life in zebra finches (Taeniopygia guttata). We found no effects of micronutrient intake on telomere loss during chick growth. However, females given a diet high in micronutrients during sexual maturation showed reduced telomere loss; there was no such effect in males. These results suggest that micronutrients may influence rates of cellular senescence, but differences in micronutrient requirement and allocation strategies, probably linked to the development of sexual coloration, may underlie sex differences in response.

Oxidative stress and life histories: unresolved issues and current needs.

Life-history theory concerns the trade-offs that mold the patterns of investment by animals between reproduction, growth, and survival. It is widely recognized that physiology plays a role in the mediation of life-history trade-offs, but the details remain obscure. As life-history theory concerns aspects of investment in the soma that influence survival, understanding the physiological basis of life histories is related, but not identical, to understanding the process of aging. One idea from the field of aging that has gained considerable traction in the area of life histories is that life-history trade-offs may be mediated by free radical production and oxidative stress. We outline here developments in this field and summarize a number of important unresolved issues that may guide future research efforts. The issues are as follows. First, different tissues and macromolecular targets of oxidative stress respond differently during reproduction. The functional significance of these changes, however, remains uncertain. Consequently there is a need for studies that link oxidative stress measurements to functional outcomes, such as survival. Second, measurements of oxidative stress are often highly invasive or terminal. Terminal studies of oxidative stress in wild animals, where detailed life-history information is available, cannot generally be performed without compromising the aims of the studies that generated the life-history data. There is a need therefore for novel non-invasive measurements of multi-tissue oxidative stress. Third, laboratory studies provide unrivaled opportunities for experimental manipulation but may fail to expose the physiology underpinning life-history effects, because of the benign laboratory environment. Fourth, the idea that oxidative stress might underlie life-history trade-offs does not make specific enough predictions that are amenable to testing. Moreover, there is a paucity of good alternative theoretical models on which contrasting predictions might be based. Fifth, there is an enormous diversity of life-history variation to test the idea that oxidative stress may be a key mediator. So far we have only scratched the surface. Broadening the scope may reveal new strategies linked to the processes of oxidative damage and repair. Finally, understanding the trade-offs in life histories and understanding the process of aging are related but not identical questions. Scientists inhabiting these two spheres of activity seldom collide, yet they have much to learn from each other.

Stress exposure in early post-natal life reduces telomere length: an experimental demonstration in a long-lived seabird.

Exposure to stressors early in life is associated with faster ageing and reduced longevity. One important mechanism that could underlie these late life effects is increased telomere loss. Telomere length in early post-natal life is an important predictor of subsequent lifespan, but the factors underpinning its variability are poorly understood. Recent human studies have linked stress exposure to increased telomere loss. These studies have of necessity been non-experimental and are consequently subjected to several confounding factors; also, being based on leucocyte populations, where cell composition is variable and some telomere restoration can occur, the extent to which these effects extend beyond the immune system has been questioned. In this study, we experimentally manipulated stress exposure early in post-natal life in nestling European shags (Phalacrocorax aristotelis) in the wild and examined the effect on telomere length in erythrocytes. Our results show that greater stress exposure during early post-natal life increases telomere loss at this life-history stage, and that such an effect is not confined to immune cells. The delayed effects of increased telomere attrition in early life could therefore give rise to a 'time bomb' that reduces longevity in the absence of any obvious phenotypic consequences early in life.