| dc.description.abstract | Breeding has a high energy requirement. Common stressors such as food restriction introduced during breeding can stimulate reproductive trade-offs by requiring more energy than the amount of energy available in the environment and further reducing that energy availability. In particular, short-lived animals may be more inclined to prioritize reproduction over self-maintenance, as they have fewer chances to breed in the future compared to long-lived animals. However, the relationship between food restriction during breeding, the outcome of reproductive trade-offs, and potential mechanisms for these trade-offs in short-lived species have proven difficult to identify, especially since directly manipulating food in the wild is nearly impossible. While there are studies that effectively restrict food and investigate reproductive trade-offs in mammals, these have rarely been identified in birds, which have higher metabolisms and generally require more daily energy than mammals. Further, if parents prioritize reproduction, they can protect their young from stressors, but this phenomenon is poorly understood. This is particularly important because developmental stressors can shape the morphology and physiology of an individual. These effects have been assumed to be permanent and consequently impact fitness. However, not all effects of developmental stressors are permanent, and repeated measures or measures of fitness are rare, thus one cannot conclude whether a stressor during development is beneficial or detrimental for the organism. Throughout my dissertation, I aimed to fill these gaps in developmental stress research and reproductive trade-offs using a model species (zebra finch, Taeniopygia castanotis) and a common stressor (food restriction). I exposed nests to either a control (ad libitum) diet or a 40% food-restricted diet when nestlings were 5 days post-hatch (dph) on average until 60 dph. To determine the effects of food restriction during breeding on the outcome and mechanisms of reproductive trade-offs, I collected samples from parents on morphology, adrenocortical and glucose responses (Chapter 2), and molecular parameters and indicators of condition (Chapter 3). To further investigate the outcomes of reproductive trade-offs and investigate the effects of chronic, developmental food restriction, I also collected samples from offspring on morphology, adrenocortical and glucose responses (Chapter 4), and development of secondary sexual characteristics and reproductive success (Chapter 5). Most of these parameters were collected at multiple time points reflecting different stages of the breeding period and development.
In parents (Chapters 2 and 3), food-restricted breeding parents had lower body mass and higher baseline corticosterone but no changes in furculum fat or glucose levels compared to controls. There was also a negative association between 1) parent body mass change and baseline corticosterone and 2) parent body mass change and offspring brood mass, but only in food-restricted birds. All effects were observed during the fledging period, which is notably the most energetically demanding period for parents. These data suggest that parents may be prioritizing their reproductive bout over somatic maintenance, and corticosterone could be a mechanism for this energy allocation. Furthermore, food-restricted breeding parents increased telomere length while controls did not alter telomere length, suggesting a robust relationship between food restriction and telomere length and an increase in cellular maintenance. I did not observe changes in DNA damage or beak coloration (an indicator of condition) during treatment. However, parents that lost more mass also had less DNA damage, suggesting that food-restricted parents may be upregulating their DNA repair mechanisms to mitigate damage to a level similar to controls.
In offspring (Chapters 4 and 5), food-restricted individuals had lower body mass only in adulthood (not during the treatment period), higher baseline corticosterone and baseline glucose, but no changes in furculum fat or growth rate. Further, there was a negative association between body mass in adulthood and baseline corticosterone in adulthood. Data from this chapter suggest that parents are buffering their offspring from the stressor, but not enough, and offspring may be utilizing corticosterone to allocate energy toward maintenance of body mass during the treatment period. Food-restricted offspring also had lower reproductive success and slower development of male cheek patches, indicating detrimental effects of chronic, developmental food restriction on fitness indices. However, there was no significant difference in beak or cheek patch color or cheek patch size in adulthood, suggesting that neither beaks nor cheek patches are honest signals of past developmental stress exposure.
Overall, these data suggest there could be a trade-off between current reproductive bout and self-maintenance where parents attempt to buffer their offspring from food restriction and allocate the remainder of their energy toward protecting their DNA. However, this may not be enough, as offspring still experience adverse effects of food restriction after treatment, even in adulthood. Therefore, examining the outcomes of reproductive trade-offs and long-term studies are important to determine the full effects of a stressor, and food restriction applied during development is overall detrimental in a short-lived passerine. | en_US |
