Physiological and Biochemical Zoology最新文献

AbstractIn vertebrates, developmental conditions can have long-term effects on individual performance. It is increasingly recognized that oxidative stress could be one physiological mechanism connecting early-life experience to adult phenotype. Accordingly, markers of oxidative status could be useful for assessing the developmental constraints encountered by offspring. Although some studies have demonstrated that developmental constraints are associated with high levels of oxidative stress in offspring, it remains unclear how growth, parental behavior, and brood competition may altogether affect oxidative stress in long-lived species in the wild. Here, we investigated this question in a long-lived Antarctic bird species by testing the impact of brood competition (e.g., brood size and hatching order) on body mass and on two markers of oxidative damage in Adélie penguin chicks. We also examined the influence of parental effort (i.e., foraging trip duration) and parental body condition on chick body mass and oxidative damage. First, we found that brood competition and parental traits had significant impacts on chick body mass. Second, we found that chick age and, to a lesser extent, chick body mass were two strong determinants of the levels of oxidative damage in Adélie penguin chicks. Finally, and importantly, we also found that brood competition significantly increased the levels of one marker of oxidative damage and was associated with a lower survival probability. However, parental effort and parental condition were not significantly linked to chick levels of oxidative damage. Overall, our study demonstrates that sibling competition can generate an oxidative cost even for this long-lived Antarctic species with a limited brood size (maximum of two chicks).

Drosophila experimental evolution, with its well-defined selection protocols, has long supplied useful genetic material for the analysis of functional physiology. While there is a long tradition of interpreting the effects of large-effect mutants physiologically, identifying and interpreting gene-to-phenotype relationships has been challenging in the genomic era, with many labs not resolving how physiological traits are affected by multiple genes throughout the genome. Drosophila experimental evolution has demonstrated that multiple phenotypes change because of the evolution of many loci across the genome, creating the scientific challenge of sifting out differentiated but noncausal loci for individual characters. The fused lasso additive model method allows us to infer some of the differentiated loci that have relatively greater causal effects on the differentiation of specific phenotypes. The experimental material that we use in the present study comes from 50 populations that have been selected for different life histories and levels of stress resistance. Differentiation of cardiac robustness, starvation resistance, desiccation resistance, lipid content, glycogen content, water content, and body masses was assayed among 40-50 of these experimentally evolved populations. Through the fused lasso additive model, we combined physiological analyses from eight parameters with whole-body pooled-seq genomic data to identify potentially causally linked genomic regions. We have identified approximately 2,176 significantly differentiated 50-kb genomic windows among our 50 populations, with 142 of those identified genomic regions that are highly likely to have a causal effect connecting specific genome sites to specific physiological characters.

AbstractEnvironmental challenges faced early in life can both activate and shape the development of the hypothalamic-pituitary-adrenal axis. Activation of this axis is characterized in part by elevated levels of glucocorticoids, exposure to which can have profound effects throughout an animal's life. We have demonstrated that in nestling eastern bluebirds (Sialia sialis), bouts of environmentally relevant cooling result in elevations of corticosterone (the primary avian glucocorticoid) very early in life. Nestlings repeatedly exposed to cooling also exhibit dampened corticosterone secretion later in life in response to restraint compared to control nestlings. We explored the mechanistic basis of this phenomenon. Specifically, we asked whether early-life cooling alters adrenal sensitivity to adrenocorticotropic hormone (ACTH), the primary controller of corticosterone synthesis and release. To this end, we subjected nestlings to repeated bouts of cooling (cooled nestlings) or brooding temperatures (control nestlings) early in life and, before fledging, assessed (1) the capacity of the nestlings' adrenals to produce corticosterone following ACTH injection, (2) the effect of cooling on corticosterone responses to restraint, and (3) the effect of cooling on adrenal sensitivity to ACTH. We found that both cooled and control nestlings secreted substantially higher levels of corticosterone following ACTH treatment than they did following restraint. We also confirmed that cooled nestlings had reduced corticosterone secretion in response to restraint compared to control nestlings; however, sensitivity to exogenous ACTH did not differ between temperature treatments. We hypothesize that early-life cooling alters later corticosterone secretion by affecting higher levels of the hypothalamic-pituitary-adrenal axis.

AbstractDuring the colonization of freshwater by marine fish, adaptation to hypoosmotic conditions may impact their ability to osmoregulate in seawater. The prickly sculpin (Cottus asper) is a euryhaline fish with marine ancestors that postglacially colonized many freshwater habitats. Previous work on C. asper suggested that isolation in freshwater habitats has resulted in putative adaptations that improve ion regulation in freshwater populations compared with populations with current access to estuaries. To determine whether long-term colonization of freshwater is associated with a reduced ability to ion regulate in seawater, we acclimated C. asper populations from three habitat types that vary in the extent to which they are isolated from marine habitats and compared their seawater osmoregulation. Seawater acclimation revealed that lake populations exhibited a reduced capacity to osmoregulate in seawater compared with coastal river populations with ongoing access to estuaries. In particular, when acclimated to seawater for several weeks, lake populations had lower gill Na⁺/K⁺-ATPase activity and lower intestinal H⁺-ATPase activity than coastal river populations. Lake populations also had a reduced ability to maintain plasma ion concentrations, and they produced lower quantities of intestinal carbonate precipitates in seawater than coastal river populations. Furthermore, there was a positive relationship between the anterior intestinal Na⁺/K⁺-ATPase activity and the amount of precipitate produced by the intestine, which suggests that the anterior intestine plays a role in seawater osmoregulation. Our results suggest that the extent of isolation from the sea could, in part, explain the reduced osmoregulation in seawater in postglacial freshwater populations of C. asper.

AbstractThe dramatic decrease in heart rate (HR) during entrance into hibernation is not a mere response to the lowering of core body temperature (T_b) but a highly regulated fall, as the decrease in HR precedes the drop in T_b. This regulated fall in HR is thought to be mediated by increased cardiac parasympathetic activity. Conversely, the sympathetic nervous system is thought to drive the increase of HR during arousal. Despite this general understanding, we lack temporal information on cardiac parasympathetic regulation throughout a complete hibernation bout. The goal of this study was to fill this gap in knowledge by using Arctic ground squirrels implanted with electrocardiogram/temperature telemetry transmitters. Short-term HR variability (root mean square of successive differences [RMSSD]), an indirect measure of cardiac parasympathetic regulation, was calculated in 11 Arctic ground squirrels. RMSSD, normalized as RMSSD/RR interval (RRI), increased fourfold during early entrance (from $0.2\pm 0.1$ to $0.8\pm 0.2$, $P<0.05$). RMSSD/RRI peaked after HR dropped by over 90% and T_b fell by 70%. Late entrance was delineated by a decline in RMSSD/RRI while T_b continued to decrease. During arousal, HR started to increase 2 h before T_b, with a concurrent decrease in RMSSD/RRI to a new minimum. As T_b increased to a maximum during interbout arousal, HR declined, and RMSSD/RRI increased. These data suggest that activation of the parasympathetic nervous system initiates and regulates the HR decrease during entrance into hibernation and that withdrawal of parasympathetic activation initiates arousal. We conclude that cardiac parasympathetic regulation persists throughout all phases of a hibernation bout-a feature of the autonomic nervous system's regulation of hibernation that was not appreciated previously.

AbstractMany attempts at providing a single-scale exponent and mechanism to explain metabolic rate assert a monolithic selective mechanism for allometries, characterized by a universal allometric scale power (usually chosen to be 0.75). To test for the deviations from universal allometric scaling, we gathered data from previously published metabolic measurements on 903 bird species and performed regressions of log(basal metabolic rate) and log(body mass) for (1) all birds and (2) 20 monophyletic clades within birds. We constructed two Bayesian linear mixed models-one included ecological variables and the other included data for mammals from Sieg et al. (2009). Overall allometric patterns differed significantly among clades of birds, and some clades were not consistent with the 0.75 scale power. We were unable to find apparent physiological, morphological, phylogenetic, or ecological characteristics among clades, predicting a difference in allometry or consistency with any previously proposed universal allometry. The Bayesian analysis illuminated novel bivariate, clade-specific differences in scaling slope-intercept space, separating large groups of birds and mammals. While significantly related to basal metabolic rate, feeding guild and migratory tendency had small effects compared to clade and body mass. We propose that allometric hypotheses, in general, must extend beyond simple overarching mechanisms to allow for conflicting and interacting influences that produce allometric patterns at narrower taxonomic scales-perhaps including other processes whose optimization may interfere with that of the system proposed by the metabolic theory of ecology.

AbstractDuring multiday torpor, deep-hibernating mammals maintain a hypometabolic state where heart rate and ventilation are reduced to 2%-4% of euthermic rates. It is hypothesized that this ischemia-like condition may cause DNA damage through reactive oxygen species production. The reason for intermittent rewarming (arousal) during hibernation might be to repair the accumulated DNA damage. Because increasing ambient temperatures (T_a's) shortens torpor bout duration, we hypothesize that hibernating at higher T_a's will result in a faster accumulation of genomic DNA damage. To test this, we kept 39 male and female garden dormice at a T_a of either 5°C or 10°C and obtained tissue at 1, 4, and 8 d in torpor to assess DNA damage and recruitment of DNA repair markers in splenocytes. DNA damage in splenocytes measured by comet assay was significantly higher in almost all torpor groups than in summer euthermic groups. Damage accumulates in the first days of torpor at $T_a=5^{°}\text{C}$ (between days 1 and 4) but not at $T_a={10}^{°}\text{C}$. At the higher T_a, DNA damage is high at 24 h in torpor, indicating either a faster buildup of DNA damage at higher T_a's or an incomplete repair during arousals in dormice. At 5°C, recruitment of the DNA repair protein 53BP1 paralleled the increase in DNA damage over time during torpor. In contrast, after 1 d in torpor at 10°C, DNA damage levels were high, but 53BP1 was not recruited to the nuclear DNA yet. The data suggest a potential mismatch in the DNA damage/repair dynamics during torpor at higher T_a's.

AbstractMuscle contractile properties are dependent on temperature: cooler temperatures generally slow contractile rates. Contraction and relaxation are driven by underlying biochemical systems, which are inherently sensitive to temperature. Carollia perspicillata, a small Neotropical bat, experiences large temperature differentials among body regions, resulting in a steep gradient in temperature along the wing. Although the bats maintain high core body temperatures during flight, the wing muscles may operate at more than 10°C below body temperature. Partially compensating for these colder operating temperatures, distal wing muscles have lower temperature sensitivities in their contractile properties, including shortening velocity, relative to the proximal pectoralis. Shortening velocity is correlated with the activity of myosin ATPase, an enzyme that drives the cross-bridge cycle. We hypothesized that the thermal properties of myofibrillar ATPase from the pectoralis and forearm muscles of the bat wing would correlate with the temperature sensitivity of those muscles. Using myofibrillar ATPases from the proximal and distal muscles, we measured enzyme activity across a range of temperatures and enzyme thermal stability after heat incubation across a range of time points. We found that forearm muscle myofibrillar ATPase was significantly less thermally stable than pectoralis myofibrillar ATPase but that there was no significant difference in the acute temperature dependence of enzyme activity between the two muscles.