Clutch size is a fundamental predictor of avian fitness, and has been widely studied from evolutionary and ecological perspectives. However, surprisingly little is known about the physiological mechanisms that integrate environmental and state dependant cues into individually variable responses in clutch size. The only formal mechanistic hypothesis for avian clutch-size determination predicts an anti-gonadal effect of prolactin (PRL) via the inhibition of luteinizing hormone (LH), and has become widely accepted despite little experimental support. I experimentally tested the PRL-based mechanistic model for clutch size determination in an avian model system, Taeniopygia guttata using two complementary approaches. The first involved the pharmacological manipulation of PRL, while the second entailed experimentally enlarging clutch size. Contrary to predictions based on the PRL-based mechanistic model, PRL, LH and clutch size were effectively uncoupled through experimental manipulation. These findings expose a serious gap in our understanding of the physiological mechanisms of clutch size, a key life history trait.
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Thesis advisor: Williams, Tony
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