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Telomeres are protective, nucleoprotein structures at the end of chromosomes that have been associated with lifespan across taxa. However, the extent to which these associations can be attributed to absolute length vs. the rate of telomere shortening prior to sampling remains unresolved. In a longitudinal study, we examined the relationship between lifespan, telomere length and the rate of telomere shortening in wild, purple-crowned fairy-wrens (Malurus coronatus coronatus). To this end, we measured telomere length using quantitative polymerase chain reaction in the blood of 59 individuals sampled as nestlings and 4-14 months thereafter, and in 141 known-age individuals sampled on average three times across adulthood. We applied within-subject centring analyses to simultaneously test for associations between lifespan and average telomere length and telomere shortening. We reveal that the rate of telomere shortening and to a lesser extent telomere length in the first year of life independently predicted lifespan, with individuals with faster shortening rates and/or shorter telomeres living less long. In contrast, in adulthood neither telomere shortening nor telomere length predicted lifespan, despite a considerably larger data set. Our results suggest that telomere length measured very early in life (during development) and longitudinal assessments of telomere shortening during the first year of life constitute more useful biomarkers of total life expectancy than either telomere length measured after development, or telomere shortening later in adulthood.

Evidence that telomere length (TL) and dynamics can be interpreted as proxy for ‘life stress’ experienced by individuals stems largely from correlational studies. We tested for effects of an experimental increase of workload on telomere dynamics by equipping male great tits (Parus major) with a 0.9 gram backpack for a full year. In addition, we analysed associations between natural life-history variation, TL and TL dynamics. Carrying 5% extra weight for a year did not significantly accelerate telomere attrition. This agrees with our earlier finding that this experiment did not affect survival or future reproduction. Apparently, great tit males were able to compensate behaviourally or physiologically for the increase in locomotion costs we imposed. We found no cross-sectional association between reproductive success and TL, but individuals with higher reproductive success (number of recruits) lost fewer telomere base pairs in the subsequent year. We used the TRF method to measure TL, which method yields a TL distribution for each sample, and the association between reproductive success and telomere loss was more pronounced in the higher percentiles of the telomere distribution, in agreement with the higher impact of ageing on longer telomeres within individuals. Individuals with longer telomeres and less telomere shortening were more likely to survive to the next breeding season, but these patterns did not reach statistical significance. Whether successful individuals are characterized by losing fewer or more base pairs from their telomeres varies between species, and we discuss aspects of ecology and social organisation that may explain this variation.

Body condition is an important concept in behaviour, evolution and conservation, commonly used as a proxy of an individual's performance, for example in the assessment of environmental impacts. Although body condition potentially encompasses a wide range of health state dimensions (nutritional, immune or hormonal status), in practice most studies operationalize body condition using a single (univariate) measure, such as fat storage. One reason for excluding additional axes of variation may be that multivariate descriptors of body condition impose statistical and analytical challenges. Structural equation modelling (SEM) is used in many fields to study questions relating multidimensional concepts, and we here explain how SEM is a useful analytical tool to describe the multivariate nature of body condition. In this 'Research Methods Guide' paper, we show how SEM can be used to resolve different challenges in analysing the multivariate nature of body condition, such as (a) variable reduction and conceptualization, (b) specifying the relationship of condition to performance metrics, (c) comparing competing causal hypothesis and (d) including many pathways in a single model to avoid stepwise modelling approaches. We illustrated the use of SEM on a real-world case study and provided R-code of worked examples as a learning tool. We compared the predictive power of SEM with conventional statistical approaches that integrate multiple variables into one condition variable: multiple regression and principal component analyses. We show that model performance on our dataset is higher when using SEM and led to more accurate and precise estimates compared to conventional approaches. We encourage researchers to consider SEM as a flexible framework to describe the multivariate nature of body condition and thus understand how it affects biological processes, thereby improving the value of body condition proxies for predicting organismal performance. Finally, we highlight that it can be useful for other multidimensional ecological concepts as well, such as immunocompetence, oxidative stress and environmental conditions.

Telomere length and telomere shortening predict survival in many organisms. This raises the question of the contribution of genetic and environmental effects to variation in these traits, which is still poorly known, particularly for telomere shortening. We used experimental (cross-fostering) and statistical (quantitative genetic “animal models”) means to disentangle and estimate genetic and environmental contributions to telomere length variation in pedigreed free-living jackdaws (Corvus monedula). Telomere length was measured twice in nestlings, at ages 4 (n = 715) and 29 days (n = 474), using telomere restriction fragment (TRF) analysis, adapted to exclude interstitial telomeric sequences. Telomere length shortened significantly over the nestling period (10.4 ± 0.3 bp day–1) and was highly phenotypically (rP = 0.95 ± 0.01) and genetically (rG > 0.99 ± 0.01) correlated within individuals. Additive genetic effects explained a major part of telomere length variation among individuals, with its heritability estimated at h2 = 0.74 on average. We note that TRF-based studies reported higher heritabilities than qPCR-based studies, and we discuss possible explanations. Parent–offspring regressions yielded similar heritability estimates for mothers and fathers when accounting for changes in paternal telomere length over life. Year effects explained a small but significant part of telomere length variation. Heritable variation for telomere shortening was low (h2 = 0.09 ± 0.11). The difference in heritability between telomere length (high) and telomere shortening (low) agrees with evolutionary theory, in that telomere shortening has stronger fitness consequences in this population. Despite the high heritability of telomere length, its evolvability, which scales the additive genetic variance by mean telomere length, was on average 0.48%. Hence, evolutionary change of telomere length due to selection is likely to be slow.

Collective behaviour often functions to avoid predation, and is therefore especially conspicuous and complex in flocks of birds under attack by raptors. However, studying collective behaviour experimentally in natural conditions is challenging. Here, we used an artificial predator, the RobotFalcon, developed after a peregrine falcon, a cosmopolitan raptor hunting a wide variety of birds. We hunted with the RobotFalcon flocks of corvids, gulls, starlings and lapwings in an agricultural area in The Netherlands, while recording the collective escape responses of the flocks with a camera. We compared collective escape responses from the RobotFalcon with those from a drone. Flocks of all species responded to the RobotFalcon most often by collectively turning, compacting and splitting in subflocks. The frequency of collective escape was highest in starlings and corvids and lowest in gulls. For starlings only, we also compared their response to a live peregrine falcon using observational data. Similar to hunts by the real falcons, the collective escape response depended on the level of predatory threat. Flocks of all species except starlings responded less often and less intensively to the drone compared to the RobotFalcon. These results give novel insights in the predator-prey dynamics between raptors and bird flocks, and illustrate how artificial predators can be used to study prey-predator interactions experimentally in the field.

Background Short leukocyte telomere length (TL) is associated with atherosclerotic cardiovascular disease. Endothelial repair plays a key role in the development of atherosclerosis. The objective was to examine associations between TL and proliferative dynamics of endothelial colony‐forming cells (ECFCs), which behave as progenitor cells displaying endothelial repair activity. Methods and Results To isolate ECFCs, we performed a clonogenic assay on blood samples from 116 participants (aged 24–94 years) in the TELARTA (Telomere in Arterial Aging) cohort study. We detected no ECFC clones in 29 (group 1), clones with no replating capacity in other 29 (group 2), and clones with replating capacity in the additional 58 (group 3). Leukocyte TL was measured by Southern blotting and ECFCs (ECFC‐TL). Age‐ and sex‐adjusted leukocyte TL (mean±SEM) was the shortest in group 1 (6.51±0.13 kb), longer in group 2 (6.69±0.13 kb), and the longest in group 3 (6.78±0.09 kb) ( P P P r =0.82; P Conclusions Individuals with longer telomeres display a higher number of self‐renewing ECFCs. Our results also indicate that leukocyte TL, as a proxy of TL dynamics in ECFCs, could be used as a surrogate marker of endothelial repair capacity in clinical and laboratory practice because of easy accessibility of leukocytes. Registration URL: https://www.clinicaltrials.gov ; Unique identifier: NCT02176941.

Birds exposed to food insecurity—defined as temporally variable access to food—respond adaptively by storing more energy. To do this, they may reduce energy allocation to other functions such as somatic maintenance and repair. To investigate this trade-off, we exposed juvenile European starlings ( Sturnus vulgaris , n = 69) to 19 weeks of either uninterrupted food availability or a regime where food was unpredictably unavailable for a 5-h period on 5 days each week. Our measures of energy storage were mass and fat scores. Our measures of somatic maintenance were the growth rate of a plucked feather, and erythrocyte telomere length (TL), measured by analysis of the terminal restriction fragment. The insecure birds were heavier than the controls, by an amount that varied over time. They also had higher fat scores. We found no evidence that they consumed more food overall, though our food consumption data were incomplete. Plucked feathers regrew more slowly in the insecure birds. TL was reduced in the insecure birds, specifically, in the longer percentiles of the within-individual TL distribution. We conclude that increased energy storage in response to food insecurity is achieved at the expense of investment in somatic maintenance and repair.

Background: Lymphopenia due to a plummeting T-cell count is a major feature of severe COVID-19. T-cell proliferation is telomere length (TL)-dependent and TL shortens with age. Older persons are disproportionally affected by severe COVID-19, and we hypothesized that those with short TL have less capacity to mount an adequate T-cell proliferative response to SARS-CoV-2. This hypothesis predicts that among older patients with COVID-19, shorter telomeres of peripheral blood mononuclear cells (PBMCs) will be associated with a lower lymphocyte count. Methods: Our sample comprised 17 COVID-19 and 21 non-COVID-19 patients, aged 87(8) (mean(SD)) and 87 (9) years, respectively. We measured TL by the Telomere Shortest Length Assay, a novel method that measures and tallies the short telomeres directly relevant to telomere-mediated biological processes. The primary analysis quantified TL as the proportion of telomeres shorter than 2 kilobases. For comparison, we also quantified TL by Southern blotting, which measures the mean length of telomeres. Results: Lymphocyte count (109/L) was 0.91 (0.42) in COVID-19 patients and 1.50(0.50) in non-COVID-19 patients (P < 0.001). In COVID-19 patients, but not in non-COVID-19 patients, lymphocyte count was inversely correlated with the proportion of telomeres shorter than 2 kilobases (P = 0.005) and positively correlated with the mean of telomeres measured by TeSLA (P = 0.03). Lymphocyte counts showed no statistically significant correlations with Southern blotting results in COVID-19 or non-COVID-19 patients. Conclusions: These results support the hypothesis that a compromised TL-dependent T-cell proliferative response contributes to lymphopenia and the resulting disproportionate severity of COVID-19 among old adults. We infer that infection with SARS-CoV-2 uncovers the limits of the TL reserves of older persons.

Immunosenescence, the decline in immune defense with age, is an important mortality source in elderly humans but little is known of immunosenescence in wild animals. We systematically reviewed and meta-analysed evidence for age-related changes in immunity in captive and free-living populations of wild species (321 effect sizes in 62 studies across 44 species of mammals, birds and reptiles). As in humans, senescence was more evident in adaptive (acquired) than innate immune functions. Declines were evident for cell function (antibody response), the relative abundance of naïve immune cells and an in vivo measure of overall immune responsiveness (local response to phytohaemagglutinin injection). Inflammatory markers increased with age, similar to chronic inflammation associated with human immunosenescence. Comparisons across taxa and captive vs free-living animals were difficult due to lack of overlap in parameters and species measured. Most studies are cross-sectional, which yields biased estimates of age-effects when immune function co-varies with survival. We therefore suggest longitudinal sampling approaches, and highlight techniques from human cohort studies that can be incorporated into ecological research. We also identify avenues to address predictions from evolutionary theory and the contribution of immunosenescence to age-related increases in disease susceptibility and mortality.

Telomere length (TL) is increasingly used as a biomarker of senescence, but measuring telomeres remains a challenge. Within tissue samples, TL varies between cells and chromosomes. Class I telomeres are (presumably static) interstitial telomeric sequences, and terminal telomeres have been divided in shorter (Class II) telomeres and ultra-long (Class III) telomeres, and the presence of the latter varies strongly between species. Class II telomeres typically shorten with age, but little is known of Class III telomere dynamics. Using multiple experimental approaches, we show great tits to have ultra-long telomeres, and we investigated age effects on Class II and III telomeres using a longitudinal approach (our method excludes Class I telomeres). In adults, TL averaged over the whole distribution did not significantly change with age. However, more detailed analyses showed that Class II TL did shorten with age, and, as in other species, the longest Class II telomeres within individuals shortened faster with age. In contrast, Class III TL did not shorten with age within individual adults. Surprisingly, we found the opposite pattern in nestlings: Class III TL shortened significantly with age, while the age effect on Class II TL was close to zero. Thus, Class III telomere length may provide information on developmental history, while Class II telomere length provides information on telomere dynamics in adulthood. These findings have practical implications for telomere studies and raise the interesting question what causes variation in TL dynamics between chromosomes within individuals and how this is related to development. This article is protected by copyright. All rights reserved.

Whether lifespan scales to age-associated changes in health and disease is an urgent question in societies with increasing lifespan. Body mass is associated with organismal functioning in many species, and often changes with age. We here tested in zebra finches whether two factors that decreased lifespan, sex and poor environmental quality, accelerated the onset of body mass declines. We subjected 597 birds for nine years to experimentally manipulated foraging costs (harsh = H, benign = B) during development (small vs large brood size) and in adulthood (easy vs hard foraging conditions) in a 2 × 2 design. This yielded four treatment combinations (HH, HB, BH, BB) for each sex. Harsh environments during development and in adulthood decreased average body mass additively. The body mass aging trajectory showed a short steep increase in early adulthood, followed by a plateau and then a decline after 5 years. This decline occurred in all groups except for HB females, which gained mass until death. Surprisingly, the onset of body mass decline was earlier in experimental groups with a longer lifespan. In contrast, the onset of body mass decline was one year earlier in females, which lived two months (4%) shorter than males. Thus, the onset of body mass aging associated positively with the sex-specific differences in lifespan, but negatively with the environmental modulation of lifespan. Thus, body mass aging trajectories did not generally scale to lifespan, and we discuss the possible causes and implications of this finding.

Early life conditions can affect individuals for life, with harsh developmental conditions resulting in lower fitness, but the underlying mechanisms are not well understood. We hypothesized that immune function may be part of the underlying mechanism, when harsh developmental conditions result in less effective immune function. We tested this hypothesis by comparing innate immune function between zebra finches (Taeniopygia guttata) in adulthood (n=230; age 108–749 days) that were reared in either small or large broods. We used this experimental background to follow up our earlier finding that finches reared in large broods have a shorter lifespan. To render a broad overview of innate immune function, we used an array of six measures: bacterial killing capacity, hemagglutination, hemolysis, haptoglobin, nitric oxide and ovotransferrin. We found no convincing evidence for effects of natal brood size on any of the six measures of innate immune function. This raised the question whether the origin of variation in immune function was genetic, and we therefore estimated heritabilities using animal models. However, we found heritability estimates to be low (range 0.04–0.11) for all measured immune variables, suggesting variation in innate immune function can largely be attributed to environmental effects independent of early-life conditions as modified by natal brood size., Summary: Developmental hardship has many long-term implications, but its effects on adult immune function are unknown. We found no effects of a developmental manipulation on innate immune function during adulthood in zebra finches.

1. Crucial to our understanding of the ageing process is identifying how traits change with age, which variables alter their ageing process and how these traits associate with fitness.2. Here we investigated metabolic ageing in outdoor-living captive zebra finches experiencing foraging costs. We longitudinally monitored 407 individuals over 6 years and collected 3,213 measurements of two independent mass-adjusted metabolic traits: basal metabolic rate (BMRm) at thermoneutral temperatures and standard metabolic rate (SMRm), measured as BMRm but at ambient temperatures below thermoneutrality.3. We define mosaic or asynchronous ageing as the difference in standardized absolute ageing rates between traits, and we estimate the degree of asynchrony using the within-individual correlation of change in trait values with age.4. BMRm decreased linearly with age, consistent with earlier reports. In contrast, SMRm increased linearly with age. The absolute standardized change with age was significantly faster for BMRm compared to SMRm, and the within-individual correlation of age related change was negligible. To the best of our knowledge, this is the first quantification of SMRm ageing, and the finding that SMRm and BMRm age in opposite directions.5. Neither metabolic rate nor metabolic ageing rate were associated with variation in life span between individuals. Moreover, experimental manipulations of environmental quality that decreased BMRm and SMRm and shortened life span by 6 months (12%) did not affect the ageing of either metabolic trait. Females lived 2 months (4%) shorter than males, but none of the metabolic traits showed sex-specific differences at any age.6. Our findings indicate, in contrast to the current view, that baseline energy requirements increase with age, because animals do not generally live in thermoneutral conditions, and illustrate the importance of studying the ageing phenotype in an ecologically realistic setting.

Recent hypotheses propose that the human placenta and chorioamniotic membranes (CAMs) experience telomere length (TL)-mediated senescence. These hypotheses are based on mean TL (mTL) measurements, but replicative senescence is triggered by short and dysfunctional telomeres, not mTL. We measured short telomeres by a vanguard method, the Telomere shortest length assay, and telomere-dysfunction-induced DNA damage foci (TIF) in placentas and CAMs between 18-week gestation and at full-term. Both the placenta and CAMs showed a buildup of short telomeres and TIFs, but not shortening of mTL from 18-weeks to full-term. In the placenta, TIFs correlated with short telomeres but not mTL. CAMs of preterm birth pregnancies with intra-amniotic infection showed shorter mTL and increased proportions of short telomeres. We conclude that the placenta and probably the CAMs undergo TL-mediated replicative aging. Further research is warranted whether TL-mediated replicative aging plays a role in all preterm births.

Broad variation in intra- and interspecific life-history traits is largely shaped by resource limitation and the ensuing allocation trade-offs that animals are forced to make. Insulin-like growth factor 1 (IGF-1), a growth-hormone-dependent peptide, may be a key player in the regulation of allocation processes. In laboratory animals, the effects of IGF-1 on growth- and development (positive), reproduction (positive), and longevity (negative) are well established. We here review the evidence on these effects in wild vertebrates, where animals are more likely to face resource limitation and other challenges. We point out the similarities and dissimilarities in patterns of IGF-1 functions obtained in these two different study settings and discuss the knowledge we need to develop a comprehensive picture of the role of IGF-1 in mediating life-history variation of wild vertebrates.

The capacity to adequately respond to (physiological) perturbations is a fundamental aspect of physiology, and may affect health and thereby Darwinian fitness. However, little is known of the degree of individual variation in this capacity in non-model organisms. The glucose tolerance test evaluates the individual's ability to regulate circulating glucose levels, and is a widely used tool in medicine and biomedical research, because glucose regulation is thought to play a role in the ageing process, among other reasons. Here, we developed an application of the intraperitoneal glucose tolerance test (IP-GTT) to be used in small birds, to test whether individuals can be characterized by their regulation of glucose levels and the effect of successive handling on such regulation. Since the IP-injection (intraperitoneal glucose injection), repeated handling and blood sampling may trigger a stress response, which involves a rise in glucose levels, we also evaluated the effects of handling protocols on glucose response. Blood glucose levels decreased immediately following an IP-injection, either vehicle or glucose loaded, and increased with successive blood sampling. Blood glucose levels peaked, on average, at 20 min post-injection (PI) and had not yet returned back to initial levels at 120 min PI. Glucose measurements taken during the IP-GTT were integrated to estimate magnitude of changes in glucose levels over time using the incremental area under the curve (AUC) up to 40 min PI. Glucose levels integrated in the AUC were significantly repeatable within individuals over months (r = 50%; 95% CI 30-79%), showing that the ability to regulate glucose differs consistently between individuals.

Key Points Question Is leukocyte telomere length associated with the natural life span of contemporary humans? Findings This cohort study included 3259 participants from 3 longitudinal studies, of whom 1525 died during the follow-up period. Leukocyte telomere length–associated mortality from noncancer causes increased as participants aged, approaching their age at death. Meaning These data suggest that leukocyte telomere length is associated with a life span limit among contemporary humans., This cohort study examines whether leukocyte telomere length is associated with the life span of contemporary humans., Importance Leukocyte telomere length (LTL) is a trait associated with risk of cardiovascular disease and cancer, the 2 major disease categories that largely define longevity in the United States. However, it remains unclear whether LTL is associated with the human life span. Objective To examine whether LTL is associated with the life span of contemporary humans. Design, Setting, and Participants This cohort study included 3259 adults of European ancestry from the Cardiovascular Health Study (CHS), Framingham Heart Study (FHS), and Women’s Health Initiative (WHI). Leukocyte telomere length was measured in 1992 and 1997 in the CHS, from 1995 to 1998 in the FHS, and from 1993 to 1998 in the WHI. Data analysis was conducted from February 2017 to December 2019. Main Outcomes and Measures Death and LTL, measured by Southern blots of the terminal restriction fragments, were the main outcomes. Cause of death was adjudicated by end point committees. Results The analyzed sample included 3259 participants (2342 [71.9%] women), with a median (range) age of 69.0 (50.0-98.0) years at blood collection. The median (range) follow-up until death was 10.9 (0.2-23.0) years in CHS, 19.7 (3.4-23.0) years in FHS, and 16.6 (0.5-20.0) years in WHI. During follow-up, there were 1525 deaths (482 [31.6%] of cardiovascular disease; 373 [24.5%] of cancer, and 670 [43.9%] of other or unknown causes). Short LTL, expressed in residual LTL, was associated with increased mortality risk. Overall, the hazard ratio for all-cause mortality for a 1-kilobase decrease in LTL was 1.34 (95% CI, 1.21-1.47). This association was stronger for noncancer causes of death (cardiovascular death: hazard ratio, 1.28; 95% CI, 1.08-1.52; cancer: hazard ratio, 1.13; 95% CI, 0.93-1.36; and other causes: hazard ratio, 1.53; 95% CI, 1.32-1.77). Conclusions and Relevance The results of this study indicate that LTL is associated with a natural life span limit in contemporary humans.

Telomere length (TL) and shortening is increasingly shown to predict variation in survival and lifespan, raising the question of what causes variation in these traits. Oxidative stress is well known to accelerate telomere attrition in vitro, but its importance in vivo is largely hypothetical. We tested this hypothesis experimentally by supplementing white stork (Ciconia ciconia) chicks with antioxidants. Individuals received either a control treatment, or a supply of tocopherol (vitamin E) and selenium, which both have antioxidant properties. The antioxidant treatment increased the concentration of tocopherol for up to two weeks after treatment but did not affect growth. Using the telomere restriction fragment technique, we evaluated erythrocyte TL and its dynamics. Telomeres shortened significantly over the 21 days between the baseline and final sample, independent of sex, mass, size and hatching order. The antioxidant treatment significantly mitigated shortening rate of average TL (−31% in shorter telomeres; percentiles 10th, 20th and 30th). Thus, our results support the hypothesis that oxidative stress shortens telomeres in vivo., Diego San Mauro for his financial support for the telomere assays (Project CGL2017-85637-P financed by the Spanish Ministry of Economy and Competitiveness). Fieldwork for this study and oxidative stress assays were partly supported by project RTA2011-00111-C03-02 financed by the Spanish National Institute for Agricultural Research INIA. J.P.-P. was funded by a grant from the Complutense University of Madrid (CT45/15-CT46/15).

Telomeres are protective caps at the end of chromosomes, and their length is positively correlated with individual health and lifespan across taxa. Longitudinal studies have provided mixed results regarding the within-individual repeatability of telomere length. While some studies suggest telomere length to be highly dynamic and sensitive to resource-demanding or stressful conditions, others suggest that between-individual differences are mostly present from birth and relatively little affected by the later environment. This dichotomy could arise from differences between species, but also from methodological issues. In our study, we used the highly reliable Terminal Restriction Fragment analysis method to measure telomeres over a 10-year period in adults of a long-lived seabird, the common tern (Sterna hirundo). Telomeres shortened with age within individuals. The individual repeatability of age-dependent telomere length was high (>0.53), and independent of the measurement interval (i.e., one vs. six years). A small (R-2 = .01), but significant part of the between-individual variation in telomere length was, however, explained by the number of fledglings produced in the previous year, while reproduction in years prior to the previous year had no effect. We confirmed that age-dependent telomere length predicted an individual's remaining lifespan. Overall, our study suggests that the majority of between-individual variation in adult telomere length is consistent across adult life, and that a smaller part of the variation can be explained by dynamic factors, such as reproduction.

Telomere length (TL) and shortening rate predict survival in many organisms. Evolutionary dynamics of TL in response to survival selection depend on the presence of genetic variation that selection can act upon. However, the amount of standing genetic variation is poorly known for both TL and TL shortening rate, and has not been studied for both traits in combination in a wild vertebrate. We used experimental (cross-fostering) and statistical (animal models) means to disentangle and estimate genetic and environmental contributions to TL variation in pedigreed free-living jackdaws (Corvus monedula). TL was measured twice early in life (age- and interval-standardized), when shortening is highest, using the high-precision TRF technique, adapted to exclude interstitial telomeric sequences. TL shortened significantly during the nestling phase (10.4 bp/day), was highly repeatable within individuals (R=0.97) and genetically correlated between the two ages (rG>0.99). Additive genetic effects explained the major part of TL variation between individuals, with heritability on average estimated ath2=0.74. Parent- offspring regressions yielded similar estimates for the sexes when accounting for changes in paternal TL over life. Cohort effects explained a small but significant part of TL variation. Heritable variation for telomere shortening was negligible. Despite the high heritability of TL, its evolvability, which scales the additive genetic variance by mean TL, was close to zero. Hence evolutionary change of TL is likely to be slow despite significant selection.

Comparability of findings from qPCR‐based telomere studies is hampered by such measurement results being assay‐specific, precluding a direct quantitative comparisons of observed differences and/or slopes of associations between studies. It is proposed that this can be partially alleviated by expressing qPCR‐based telomere data as Z‐scores.

Most of our knowledge about the regulation and function of sleep is based on studies in a restricted number of mammalian species, particularly nocturnal rodents. Hence, there is still much to learn from comparative studies in other species. Birds are interesting because they appear to share key aspects of sleep with mammals, including the presence of two different forms of sleep, i.e. non-rapid eye movement (NREM) and rapid eye movement (REM) sleep. We examined sleep architecture and sleep homeostasis in the European starling, using miniature dataloggers for electroencephalogram (EEG) recordings. Under controlled laboratory conditions with a 12:12 h light–dark cycle, the birds displayed a pronounced daily rhythm in sleep and wakefulness with most sleep occurring during the dark phase. Sleep mainly consisted of NREM sleep. In fact, the amount of REM sleep added up to only 1~2% of total sleep time. Animals were subjected to 4 or 8 h sleep deprivation to assess sleep homeostatic responses. Sleep deprivation induced changes in subsequent NREM sleep EEG spectral qualities for several hours, with increased spectral power from 1.17 Hz up to at least 25 Hz. In contrast, power below 1.17 Hz was decreased after sleep deprivation. Sleep deprivation also resulted in a small compensatory increase in NREM sleep time the next day. Changes in EEG spectral power and sleep time were largely similar after 4 and 8 h sleep deprivation. REM sleep was not noticeably compensated after sleep deprivation. In conclusion, starlings display signs of NREM sleep homeostasis but the results do not support the notion of important REM sleep functions., Sleep, 43 (6), ISSN:1550-9109, ISSN:0161-8105

The integration and synthesis of the data in different areas of science is drastically slowed and hindered by a lack of standards and networking programmes. Long-term studies of individually marked animals are not an exception. These studies are especially important as instrumental for understanding evolutionary and eco-logical processes in the wild. Furthermore, their number and global distribution provides a unique opportunity to assess the generality of patterns and to address broad-scale global issues (e.g. climate change)., To solve data integration issues and enable a new scale of ecological and evolution-ary research based on long-term studies of birds, we have created the SPI-Birds Network and Database (www.spibirds.org)—a large-scale initiative that connects data from, and researchers working on, studies of wild populations of individually recognizable (usually ringed) birds. Within year and a half since the establishment, SPI-Birds has recruited over 120 members, and currently hosts data on almost 1.5 million individual birds collected in 80 populations over 2,000 cumulative years, and counting., SPI-Birds acts as a data hub and a catalogue of studied populations. It prevents data loss, secures easy data finding, use and integration and thus facilitates collab-oration and synthesis. We provide community-derived data and meta-data stand-ards and improve data integrity guided by the principles of Findable, Accessible, Interoperable and Reusable (FAIR), and aligned with the existing metadata lan-guages (e.g. ecological meta-data language)., The encouraging community involvement stems from SPI-Bird's decentralized ap-proach: research groups retain full control over data use and their way of data management, while SPI-Birds creates tailored pipelines to convert each unique data format into a standard format. We outline the lessons learned, so that other communities (e.g. those working on other taxa) can adapt our successful model. Creating community-specific hubs (such as ours, COMADRE for animal demogra-phy, etc.) will aid much-needed large-scale ecological data integration., The SPI-Birds have been supported by an NWO personal grant (grant number 016.Veni.181.054) to A.C., and a Research Council of Norway grant: 223257 (SFF-III) and 267511 (EVOCLIM).

Ecological conditions affect fitness, but mechanisms causing such effects are not well known, while evolved responses to environmental variation may depend on the underlying mechanisms. Consequences of environmental conditions vary strongly between traits, but a framework to interpret such variation is lacking. We propose that variation in trait response may be explained by differential canalisation, with traits with larger fitness effects showing weaker responses to environmental perturbations due to preferential resource allocation to such traits. We tested the canalisation hypothesis using brood size manipulation in wild jackdaw nestlings in which we measured eight physiological traits (mainly oxidative stress markers), and two feather traits. For each trait, we estimated manipulation response and association with fitness (over-winter survival). As predicted, a strong negative correlation emerged between manipulation response and association with fitness (r = -0.76). We discuss the consequences of differential trait canalisation for the study of mechanisms mediating environmental effects on fitness.

High baseline glucose levels are associated with pathologies and shorter lifespan in humans, but little is known about causes and consequences of individual variation in glucose levels in other species. We tested to what extent baseline blood glucose level is a repeatable trait in adult zebra finches, and whether glucose levels were associated with age, manipulated environmental conditions during development (rearing brood size) and adulthood (foraging cost), and lifespan. We found that: (1) repeatability of glucose levels was 30%, both within and between years. (2) Having been reared in a large brood and living with higher foraging costs as adult were independently associated with higher glucose levels. Furthermore, the finding that baseline glucose was low when ambient temperature was high, and foraging costs were low, indicates that glucose is regulated at a lower level when energy turnover is low. (3) Survival probability decreased with increasing baseline glucose. We conclude that baseline glucose is an individual trait negatively associated with survival, and increases due to adverse environmental conditions during development (rearing brood size) and adulthood (foraging cost). Blood glucose may be, therefore, part of the physiological processes linking environmental conditions to lifespan.

International audience; Telomere length (TL) trajectories in somatic tissues during human growth and development are poorly understood. We examined a blood-and-muscle model during early life, focusing on TL trajectories in leukocytes, representing the highly proliferative hematopoietic system, and skeletal muscle, a minimally proliferative tissue. Leukocyte TL (LTL) and skeletal muscle TL (MTL) were measured in 28 fetuses and 73 children. LTL and MTL were highly variable across individuals (sd: fetal LTL = 0.72 kb, MTL = 0.72 kb; children LTL = 0.81 kb, MTL = 0.82 kb) but were highly correlated within individuals (fetuses, r = 0.76, P < 0.0001; children, r = 0.87, P < 0.0001). LTL was shorter than MTL in fetuses (10.63 vs. 11.01 kb; P = 0.0004) and children (8.46 vs. 9.40 kb

As attrition of telomeres, DNA caps that protect chromosome integrity, is accelerated by various forms of stress, telomere length (TL) has been proposed as an indicator of lifetime accumulated stress. In ecological studies, it has been used to provide insights into ageing, life history trade-offs, the costs of reproduction and disease. qPCR is a high-throughput and cost-effective tool to measure relative TL (rTL) that can be applied to newly collected and archived ecological samples. However, qPCR is susceptible to error both from the method itself and pre-analytical steps. Here, repeatability was assessed overall and separately across multiple levels (intra-assay, inter-assay and inter-extraction) to elucidate the causes of measurement error, as a step towards improving precision. We also tested how accuracy, defined as the correlation between the "gold standard" for TL estimation (telomere restriction fragment length analysis with in-gel hybridization), could be improved. We find qPCR repeatability (intra- and inter-assay levels) to be at similar levels across three common storage media (ethanol, Longmire's and Queen's). However, inter-extraction repeatability was 50% lower for samples stored in Queen's lysis buffer, indicating storage medium can influence precision. Precision as well as accuracy could be increased by estimating rTL from multiple qPCR reactions and from multiple extractions. Repetition increased statistical power equivalent to a 25% (single extraction analysed twice) and 17% (two extractions) increase in sample size. Overall, this study identifies novel sources of variability in high-throughput telomere quantification and provides guidance on sampling strategy design and how to increase rTL precision and accuracy.

Basal metabolic rate (BMR) is often assumed to be indicative of the energy turnover at ambient temperatures (Ta) below the thermoneutral zone (SMR), but this assumption has remained largely untested. Using a new statistical approach, we quantified the consistency in nocturnal metabolic rate across a temperature range in zebra finches (n=3,213 measurements on 407 individuals) living permanently in eight outdoor aviaries. Foraging conditions were either benign or harsh, and body mass and mass-adjusted BMRm and SMRm were lower in individuals living in a harsh foraging environment. The correlation between SMRm at different Tas was high (r=0.91), independent of foraging environment, showing that individuals are consistently ranked according to their SMRm. However, the correlations between BMRm and SMRm were always lower (average: 0.29; range: 0

Developmental conditions in early life frequently have long-term consequences on the adult phenotype, but the adult environment can modulate such long-term effects. Glucocorticoid hormones may be instrumental in mediating developmental effects, but the permanency of such endocrine changes is still debated. Here, we manipulated environmental conditions during development (small vs. large brood size, and hence sibling competition) and in adulthood (easy vs. hard foraging conditions) in a full factorial design in zebra finches, and studied effects on baseline (Bas-COAT) and stress-induced (SI-CORT) corticosterone in adulthood. Treatments affected Bas-CORT in females, but not in males. Females reared in small broods had intermediate Bas-CORT levels as adults, regardless of foraging conditions in adulthood, while females reared in large broods showed higher Bas-CORT levels in hard foraging conditions and lower levels in easy foraging conditions. Female Bas-CORT was also more susceptible than male Bas-COAT to non-biological variables, such as ambient temperature. In line with these results, repeatability of Bas-CORT was higher in males (up to 51%) than in females (25%). SI-CORT was not responsive to the experimental manipulations in either sex and its repeatability was high in both sexes. We conclude that Bas-CORT responsiveness to intrinsic and extrinsic conditions is higher in females than in males, and that the expression of developmental conditions may depend on the adult environment. The latter finding illustrates the critical importance of studying of causes and consequences of long-term developmental effects in other environments in addition to standard laboratory conditions. (C) 2017 Published by Elsevier Inc.

Summary 1.Biomarkers that predict fitness are instrumental in unravelling mechanisms that link environmental conditions to fitness. However, development is likely to be better canalized for traits with stronger fitness effects. As a consequence, traits that are sensitive to developmental conditions may be poor fitness predictors and vice versa, and we tested for such effects using feather fault bars (translucent areas on feathers associated with developmental stress) in nestling birds. 2.We manipulated developmental conditions (brood size) in free-living jackdaws (Coloeus monedula) and compared the effect on fault bar number between two feather types, tail and wing coverts. Fault bar number in the two feather types correlated poorly, indicating they can be considered different traits. Subsequently, we monitored local survival to investigate how well both traits linked developmental conditions to survival prospects. 3.Tail fault bar number reflected developmental conditions better than the number of fault bars in the wings: when pre-manipulation brood size was small, nestlings had more tail fault bars when brood size was subsequently enlarged, while there was no such manipulation effect on the number of fault bars in wing coverts. 4.In contrast, fault bar number in wing coverts better predicted fledgling local survival compared to tail coverts. 5.We conclude that fault bar number in tail coverts is a biomarker of developmental conditions, while fault bar number in wing coverts is a predictor of survival prospects, but neither trait successfully links developmental conditions to fitness prospects. These findings are in agreement with the expectation that development of traits with a stronger relation to fitness will be better canalized. We discuss three hypotheses that can explain why despite canalization there are traits that are both sensitive to developmental conditions and predict fitness prospects. This article is protected by copyright. All rights reserved.