Amphibian metamorphosis involves a complex but coordinate transformation of individual tissues in a tadpole. It is becoming increasingly clear that thyroid hormone controls metamorphosis by regulating a cascade of gene expression in this process. Thus, the overall objective of my thesis was to establish whether or not thyroid hormone induces the expression of one or more of the actin genes in the heart or other tissues/organs of the metamorphosing Rana catesbeiana (American bullfrog) tadpole. In order to accomplish my objective, I isolated and characterized the cDNAs and genomic DNAs encoding various isoforms of actin in this amphibian and, subsequently, evaluated the expression of the genes encoding these actin isoforms.

The complete regression of a tadpole's tail during its transition to a frog is dramatic and a morphological hallmark of amphibian metamorphosis. Studies of tail regression indicate that the destruction of this organ involves a genetic program which is initiated by thyroid hormone and consists of several phases, all of which are thought to involve changes in gene expression. Previous studies, focused on the initial phase of tail regression in the Rana catesbeiana tadpole, have shown that a decrease in the rate of synthesis of some myofibrillar proteins, such as the myosin heavy chains, is an early, thyroid hormone-mediated event. However, the question of whether this event results from regulatory mechanisms operating at the level of transcription and/or translation has not been addressed. Thus, the overall objective of my studies was to establish what effect thyroid hormone has on the expression of mRNAs encoding the heavy chains of myosin in the tail muscle of hormone-treated tadpoles, and, to accomplish my objective, I first had to isolate and characterize cDNAs encoding the myosin heavy chains found in the tail muscle of this tadpole. The results of my investigations demonstrate (1) that the genes which encode at least five of the myosin heavy chains expressed in the tadpole tail muscle are also expressed in the hindlimb muscles of tadpoles at metamorphic climax and in the limb muscles of adult frogs, (2) that thyroid hormone treatment of the tadpole does not repress the level of these mRNAs in its tail, but, instead, appears to promote an accumulation in the level of at least four of the mRNAs encoding these myosin heavy chains, and (3) that the thyroid hormone-induced up-regulation in the levels of the myosin heavy chain mRNAs is early and coincidental with an up-regulation in the levels of mRNAs encoding TR$\alpha,$ TR$\beta$ and the Rana homologue of a mammalian C/EBP-$\delta.$ These results suggest that the thyroid hormone-induced decrease in the rate of myosin heavy chain synthesis in the tadpole tail muscle is not related to a depression in the amount of mRNAs encoding the tadpole (stage-specific) isoforms of the myosin heavy chains.