Thyroid hormone deiodinases revisited : insights from lungfish : a review

In vertebrates, hormones released from the thyroid gland travel in the circulation to target tissues where they may be processed by deiodinating enzymes into more active or inactive iodothyronines. In mammals, there are three deiodinating enzymes described. Type1 (D1), which primarily occurs in the liver, converts reverse T3 into T2 for clearance. It also converts T4 into T3. This production of T3 is believed to contribute to the bulk of circulating T3 in mammals. The type2 (D2) enzyme may be found in many other tissues where it converts T4 to T3, which is then transferred to the receptors in the nucleus of the same cell, i.e. does not contribute to the circulating T3. The type3 (D3) enzyme converts T3 into T2. The expression of the genes for these three enzymes and/or the activity of the enzymes have been studied in several non-mammalian groups of vertebrates. From agnathans to birds, D2 and D3 appear to occur universally, with the possible exception of squamate reptiles (lack D2?). D1 has not been found in amphibians, lungfish or agnathans. All three enzymes are selenoproteins, in which a selenocysteine is found in the active centre. The nucleotide code for translation of a selenocysteine is UGA, which under normal circumstances is a stop codon. In order for UGA to code for selenocysteine, there must be a SECIS element in the 3'UTR of the mRNA. Any disruption of the SECIS will result in a truncated protein in the region of its active centre. It is suggested that such alternative splicing may be a mode of altering the expression of deiodinases in particular tissues to change the response of such tissues to thyroid hormones under differing circumstances such as stages of development.6 page(s

Tuning crystalline ordering by annealing and additives to study its effect on exciton diffusion in a polyalkylthiophene copolymer

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Molecular and cellular changes in skin and muscle during metamorphosis of Atlantic halibut (Hippoglossus hippoglossus) are accompanied by changes in deiodinases expression

Flatfish metamorphosis is the most dramatic postnatal developmental event in teleosts. Thyroid hormones (TH), thyroxine (T4) and 3,3′-5′-triiodothyronine (T3) are the necessary and sufficient factors that induce and regulate flatfish metamorphosis. Most of the cellular and molecular action of TH is directed through the binding of T3 to thyroid nuclear receptors bound to promoters with consequent changes in the expression of target genes. The conversion of T4 to T3 and nuclear availability of T3 depends on the expression and activity of a family of 3 selenocysteine deiodinases that activate T4 into T3 or degrade T4 and T3.We thank Heiddis Smáradóttir of Fiskeldi Eyjafjarðar, IS-600 Akureyri, Iceland, for providing the halibut samples. This project was supported by the European Community project, LIFECYCLE (222719-2) and the Portuguese Ministry of Science (FCT; project PDCT/MAR/115005/2009). M.A.C. was sponsored by the Portuguese Ministry of Science (grant no. SFRH/BPD/66808/2009)