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Corticosterone-mediated reproductive decisions: sex allocation, the cost of reproduction and maternal fitness

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(Thesis) Ph.D.
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Managing reproductive investment within the scope of an individual’s energetic condition is required to maximize fitness. To be successful, individuals must make the correct decisions about when to reproduce, when to abandon an attempt, how many resources to invest in current and future attempts and where those resources should be allocated. These reproductive decisions therefore involve complex life-history trade-offs between an individual’s condition and current reproduction, future reproduction, and survival. However, how the decisions are physiologically mediated to balance these trade-offs and maximize fitness is not well understood. This thesis examines how the stress hormone corticosterone mediates reproductive decisions and asks how offspring and maternal fitness are affected by individual variation in corticosterone using an avian model, the European starling (Sturnus vulgaris). Because corticosterone maintains daily homeostatic energetic balance, it is correlated with individual energetic condition and is therefore a potential hormonal link between maternal and offspring quality. In starlings, intra-specific variation in plasma corticosterone is related to maternal condition and high baseline levels are associated with nest abandonment. Elevated maternal corticosterone is also transferred to eggs via the yolk, and intra- and inter-clutch variation in yolk corticosterone are high and significantly negatively related to maternal quality, indicating that yolk corticosterone may cue offspring to variation in maternal quality. Indeed, experimentally elevated yolk corticosterone selectively decreases male offspring quality and increases pre- and post-natal male mortality. For the mother, the result is an allocation towards evolutionarily less-expensive daughters and a sex-specific lowering of current reproductive investment. This energy-savings increases investment in future fecundity and increases maternal survival. Finally, the quality of the maternal environment can cause both pre-natal programming and post-natal plasticity in the adrenocortical axis of their offspring. This thesis has revealed that individual variation in maternal quality as mediated by corticosterone has significant and potentially sex-specific proximate effects on offspring. Exposing offspring to the effects of maternal corticosterone plays adaptive roles at multiple reproductive stages and ultimately increases maternal fitness. Together, the work here provides an evolutionary framework for how maternal stress hormones can mediate multiple reproductive decisions and life-history trade-offs in vertebrates.
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