Thyroid hormone regulation of iodothyronine deiodinase and thyroid hormone receptor transcripts in parrotfish


Meeting Abstract

P1.36  Tuesday, Jan. 4  Thyroid hormone regulation of iodothyronine deiodinase and thyroid hormone receptor transcripts in parrotfish JOHNSON, K.M.; LEMA, S.C.*; Univ. of North Carolina, Wilmington; Univ. of North Carolina, Wilmington lemas@uncw.edu

Thyroid hormones play key roles in regulating development and growth, reproduction, osmoregulation and behaviors associated with rheotaxis and migration in fish. These diverse functions are mediated at the peripheral tissue level by both iodothyronine deiodinase enzymes and the type and density of thyroid hormone receptors. In mammals, expression patterns of deiodinase enzymes and thyroid hormone receptors have been shown to be thyroid hormone regulated, but considerably less is known about expressional regulation of these pathways in teleost fish even though the pathways are increasingly used as indicators for thyroid disruption by environmental pollutants. Here, we examined thyroid hormone regulation of mRNAs encoding thyroid hormone receptors TRα A, TRα B, and TRβ, and the three deiodinase enzymes dio1, dio2, and dio3 in striped parrotfish (Scarus iserti). Initial phase parrotfish were collected from the coral reefs of Curacao and treated with dissolved phase T3 (20 nM) or methimazole (3 mM) for 3 days. In both sexes of parrotfish, exogenous T3 elevated circulating total T3, while methimazole depressed plasma total T4. The experimentally-induced hyperthyroidism increased transcription of mRNAs for TRα A and TRβ in the liver and brain, without changing TRα B transcript abundance in either tissue. In both sexes, methimazole-induced hypothyroidism elevated dio2 mRNAs in liver and brain, suggesting enhanced outer-ring deiodination activity. Hyperthyroidism, in contrast, elevated dio3 mRNA levels in these same tissues. Dio1 transcripts were unaltered by either hyper- or hypothyroidism in any tissue. These results demonstrate differential transcriptional regulation of thyroid hormone receptor isoforms and provide support for dio1 having a regulatory mechanism distinct from that observed in mammals.

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