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Thyroxine is arguably the most important hormone in anuran development and affects development through exogenous and endogenous means. In this study, I investigate the relationship between exogenous thyroxine and spadefoot tadpole development. Tadpoles of the spadefoot toad Spea multiplicata can display either a "typical" omnivorous phenotype or a carnivorous phenotype. Exogenous thyroxine and feeding on conspecific tadpoles was first proposed as the proximate mechanisms for developmental polyphenism in these tadpoles 20 years ago. Recent research on the effects of exogenous thyroxine on anuran development are at odds with the current understanding of the role of exogenous thyroxine on developmental polyphenism is spadefoot toad tadpoles. Understanding the proximate mechanism of ontogenetic polyphenism is the first step in gaining a mechanistic and evolutionary understanding of the factors responsible for the control and evolution of polyphenism. Here, I demonstrate that neither exogenous thyroxine nor feeding on conspecific tadpoles triggers developmental polyphenism in spadefoot toad larvae and show how heterochronic processes, and past reliance on ratios rather than developmental trajectories, mislead us into believing that these proximate mechanisms controlled developmental polyphenism in spadefoot toads. I also investigate comparative development of four species of spadefoot toad with and without thyroxine treatment to speculate on the controlling factors that may be responsible for general differences in development between the species. By controlling the amount of thyroxine that acts on metamorphic tissues during development, I am able to suggest that differences in development between the four species may be due to cell specific differences in receptor or metamorphic gene activity in addition to possible differences in amount of circulating thyroid hormone (thyroxine).
A Thesis Submitted to the Department of Biological Science in Partial Fulfillment of the Requirements for the Degree of Masters of Science.
Includes bibliographical references.
Florida State University
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