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Global warming is one of the primary drivers of habitat loss and population decline in numerous species, including birds, amphibians and marine life. Avian embryos exhibit ectothermic phenotypes during most of their incubation period and are also vulnerable to rising temperatures when parents cannot cool the nests. This vulnerability stems from their unique respiratory mechanisms, which utilize eggshell pores to exchange respiratory gases. The number of pores is fixed at oviposition, and embryos may experience hypoxia during later developmental stages, especially when exposed to elevated ambient/incubation temperatures. Our preliminary study on zebra finch (Taeniopygia guttata castanotis) embryos, where we covered 30% of the shell surface with beeswax and incubated at high (38.9°C) temperature, revealed that half of the individuals that failed to hatch had developed oedema in the hind neck region. This study shows that such physical anomalies occur during incubation prior to death. We found that embryos with oedema had a higher head-to-body ratio, independent of their relative brain mass. Furthermore, oedema formation was correlated with darker-coloured hearts, suggesting reduced blood oxygenation in these embryos. These results highlight the physiological challenges embryos face under suboptimal incubation conditions. This article is part of the theme issue ‘The biology of the avian respiratory system’. 

The ability for traits to recover after exposure to stress varies depending on the magnitude, duration, or type of stressor. One such stressor is circadian rhythm disruption stemming from exposure to light at night. Circadian rhythm disruption may lead to long-term physiological consequences; however, the capacity in which individuals recover and display stress resilience is not known. Here, we exposed zebra finches (Taeniopygia castanotis) to constant light (24L:0D) or a regular light/dark cycle (14L:10D) for 23 days, followed by a recovery period for 12 days. We measured body mass, corticosterone, and glucose levels at multiple timepoints, and relative protein expression of glucocorticoid receptors at euthanasia. Body mass significantly increased over time in light-exposed birds compared to controls, but a 12-day recovery period reversed this increase. Baseline levels of circulating glucose decreased in light-exposed birds compared to controls, but returned to pretreatment levels after the 12-day recovery period. In contrast, the glucose stress response did not show a similar recovery trend, suggesting longer recovery is needed or that this is a persistent effect in light-exposed birds. Surprisingly, we did not detect any differences in baseline corticosterone or reactivity of the hypothalamic-pituitiary-adrenal (HPA) axis between groups throughout the experiment. Moreover, we did not detect differences between relative protein expression of glucocorticoid receptors or a relationship with HPA axis reactivity. Yet, we found a positive relationship between glucocorticoid receptors and the glucose stress response, but only in the light group. Our results indicate that physiological and morphological traits differ in their ability to recover in response to constant light and warrants further investigation on the mechanisms driving stress resilience under a disrupted circadian rhythm. 

Synopsis Climate resilience, a focus of many recent studies, has been examined from ecological, physiological, and evolutionary perspectives. However, sampling biases toward adults, males, and certain species have made establishing the link between environmental change and population-level change problematic. Here, we used data from four laboratory studies, in which we administered pre- and postnatal stressors, such as suboptimal incubation temperature, heat stress, and food restriction, to zebra finches. We then quantified hatching success, posthatch survival, and reproductive success, to parameterize age-structured population dynamics models with the goal of estimating the effect of the stressors on relative population growth rates. Using the same model structure, we tested the hypothesis that early life stages influence population growth rate more than later life stages. Our models suggested that stressful events during embryonic development, such as suboptimal incubation temperatures and reduced gas exchange for the embryos, have a greater total impact on population growth than posthatch stressors, such as heat stress and food restriction. However, among life history traits, differences in hatching success and sex ratio of offspring in response to stressors changed population growth rates more than differences in any other demographic rate estimates. These results suggest that when predicting population resilience against climate change, it is critical to account for effects of climate change on all life stages, including early stages of life, and to incorporate individuals’ physiology and stress tolerance that likely influence future stress responses, reproduction, and survival. 

ABSTRACT Developing animals display a tremendous ability to change the course of their developmental path in response to the environment they experience, a concept referred to as developmental plasticity. This change in behavior, physiology or cellular processes is primarily thought to allow animals to better accommodate themselves to the surrounding environment. However, existing data on developmental stress and whether it brings about beneficial or detrimental outcomes show conflicting results. There are several well-referred hypotheses related to developmental stress in the current literature, such as the environmental matching, silver spoon and thrifty phenotype hypotheses. These hypotheses speculate that the early-life environment defines the capacity of the physiological functions and behavioral tendencies and that this change is permanent and impacts the fitness of the individual. These hypotheses also postulate there is a trade-off among organ systems and physiological functions when resources are insufficient. Published data on avian taxa show that some effects of developmental nutritional and thermal stressors are long lasting, such as the effects on body mass and birdsong. Although hypotheses on developmental stress are based on fitness components, data on reproduction and survival are scarce, making it difficult to determine which hypothesis these data support. Furthermore, most physiological and performance measures are collected only once; thus, the physiological mechanisms remain undertested. Here, we offer potential avenues of research to identify reasons behind the contrasting results in developmental stress research and possible ways to determine whether developmental programming due to stressors is beneficial or detrimental, including quantifying reproduction and survival in multiple environments, measuring temporal changes in physiological variables and testing for stress resistance later in life. 

The insulin and insulin-like signalling (IIS) network plays an important role in mediating several life-history traits, including growth, reproduction and senescence. Although insulin-like growth factors (IGFs) 1 and 2 are both key hormones in the vertebrate IIS network, research on IGF2 in juveniles and adults has been largely neglected because early biomedical research on rodents found negligible IGF2 postnatal expression. Here, we challenge this assumption and ask to what degree IGF2 is expressed during postnatal life across amniotes by quantifying the relative gene expression of IGF1 and IGF2 using publicly available RNAseq data for 82 amniote species and quantitative polymerase chain reaction on liver cDNA at embryonic, juvenile and adult stages for two lizard, bird and mouse species. We found that (i) IGF2 is expressed postnatally across amniote species and life stages—often at a higher relative expression than IGF1 , contradicting rodent models; (ii) the lack of rodent postnatal IGF2 expression is due to phylogenetic placement, not inbreeding or artificial selection; and (iii) adult IGF2 expression is sex-biased in some species. Our results demonstrate that IGF2 expression is typical for amniotes throughout life, suggesting that a comprehensive understanding of the mechanisms mediating variation in life-history traits will require studies that measure both IGFs. 

Abstract Why do some biological systems and communities persist while others fail? Robustness, a system's stability, and resilience, the ability to return to a stable state, are key concepts that span multiple disciplines within and outside the biological sciences. Discovering and applying common rules that govern the robustness and resilience of biological systems is a critical step toward creating solutions for species survival in the face of climate change, as well as the for the ever-increasing need for food, health, and energy for human populations. We propose that network theory provides a framework for universal scalable mathematical models to describe robustness and resilience and the relationship between them, and hypothesize that resilience at lower organization levels contribute to robust systems. Insightful models of biological systems can be generated by quantifying the mechanisms of redundancy, diversity, and connectivity of networks, from biochemical processes to ecosystems. These models provide pathways towards understanding how evolvability can both contribute to and result from robustness and resilience under dynamic conditions. We now have an abundance of data from model and non-model systems and the technological and computational advances for studying complex systems. Several conceptual and policy advances will allow the research community to elucidate the rules of robustness and resilience. Conceptually, a common language and data structure that can be applied across levels of biological organization needs to be developed. Policy advances such as cross-disciplinary funding mechanisms, access to affordable computational capacity, and the integration of network theory and computer science within the standard biological science curriculum will provide the needed research environments. This new understanding of biological systems will allow us to derive ever more useful forecasts of biological behaviors and revolutionize the engineering of biological systems that can survive changing environments or disease, navigate the deepest oceans, or sustain life throughout the solar system. 

Abstract 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. 

Abstract 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.