Developing animals respond to variation in their habitat by altering their rate of development and/or their morphology; i.e., they exhibit developmental plasticity. One mechanism by which plasticity is expressed is through activation of the neuroendocrine system, which transduces environmental information into a physiological response. Recent findings of ours with amphibians and others with mammals show that the primary vertebrate stress neuropeptide, corticotropin-releasing hormone (CRH) is essential for adaptive developmental responses to environmental stress. For instance, CRH dependent mechanisms cause accelerated metamorphosis in response to habitat desiccation stress in some amphibian species, and intrauterine fetal stress syndromes in humans precipitate preterm birth. The objectives of the proposed research are to analyze the cellular and molecular mechanisms of CRH signaling during vertebrate development. Tadpoles of the South African clawed frog Xenopus laevis will be used as the model organism. The results of these studies will provide basic information on the molecular and functional organization of this essential developmental regulatory system. Furthermore, these studies should lay a foundation for understanding the mechanistic basis of developmental responses to changes in the physical and chemical environment. Basic knowledge gained from these studies should allow a more informed and detailed understanding of normal pathways of endocrine control, knowledge that will be essential to elucidating the mechanisms by which environmental endocrine disrupters act to alter developmental processes. Such a goal is particularly cogent given recent reports of worldwide declines in amphibian populations and concerns over the effects of hormone mimicking industrial compounds on the development of humans and wild animals.
