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Low-Temperature Arrest of the Triiodothyronine-Dependent Transcription in Rana catesbeiana Red Blood Cells

Department of Biology, Faculty of Science, Shizuoka University, Shizuoka 422-8529, Japan

Address all correspondence and requests for reprints to: Dr. Kiyoshi Yamauchi, Department of Biology, Faculty of Science, Shizuoka University, 836 Ohya, Shizuoka 422-8529, Japan. E-mail: sbkyama{at}ipc.shizuoka.ac.jp.

We examined possible molecular mechanisms for the low-temperature arrest of T₃-induced Rana catesbeiana metamorphosis. Scatchard plots revealed that the ratios of maximum binding capacity/dissociation constant for high-affinity sites of tadpole serum proteins for T₃ at 20 and 28 C was 3.3–4.6 times less than that at 4 C, due to the decrease in maximum binding capacity values. Kinetic studies of T₃ uptake into tadpole red blood cells demonstrated that the ratio of maximum uptake rate/Michaelis constant at 23 C was approximately 13 times greater than that at 4 C. The process of intracellular transport of T₃ into the nucleus was not arrested at 4 C. The ratio of T₃ incorporated into nuclei to that taken up into red blood cells was not significantly different at 4, 20, and 28 C, indicating the absence of temperature-sensitive sites in this process. T₃ binding to the T₃ receptors and ß were not temperature sensitive at least at 4 and 20 C. Transcription of the tr genes, early primary T₃ response genes, was activated by 10 nM T₃ at 20 and 28 C but was barely detected at 4 C. These results indicate that the major molecular event causing the low-temperature arrest of amphibian metamorphosis occurs after T₃ entry into the nucleus but before or during the transcriptional activation of the tr genes. Plasma proteins binding T₃ and the cellular thyroid hormone uptake system on the plasma membrane may contribute to the slowing of the incorporation of T₃ into nucleus at 4 C by decreasing the uptake velocity of T₃.