Molecular characterization, gene expression and transcriptional regulation of thyroid hormone receptors in Senegalese sole
Abstract Thyroid hormones (THs) play a key role in larval development, growth and metamorphosis in flatfish. Their genomic effects are mediated by thyroid hormone receptors (TRs). In this study, cDNAs encoding for TRαA, TRαB, and TRβ have been sequenced in Senegalese sole ( Solea senegalensis ). Mai...
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Veröffentlicht in: | General and comparative endocrinology 2009-01, Vol.160 (2), p.139-147 |
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Format: | Artikel |
Sprache: | eng |
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Zusammenfassung: | Abstract Thyroid hormones (THs) play a key role in larval development, growth and metamorphosis in flatfish. Their genomic effects are mediated by thyroid hormone receptors (TRs). In this study, cDNAs encoding for TRαA, TRαB, and TRβ have been sequenced in Senegalese sole ( Solea senegalensis ). Main domains and conserved motifs were identified. Also, a truncated TRαB isoform (referred to as TRαBtr) and a spliced TRβ variant (referred to as TRβv) were detected. A phylogenetic analysis grouped both TRα and TRβ genes into two separate clusters with their fish and mammalian counterparts. Expression profiles during larval development and in juvenile tissues were analyzed using a real-time PCR approach. In juvenile fish, TRαA, TRαB, TRβv, and TRβ showed distinct transcript levels in tissues. During metamorphosis, only TRβv and TRβ modified their mRNA levels in a similar way to the T4 contents. To evaluate the possible regulation of TRs by their cognate ligand T4 during sole metamorphosis, larvae were exposed to the goitrogen thiourea (TU). TRβ transcripts decreased significantly at 11 and 15 days after treatment. Moreover, adding exogenous T4 hormone to TU-treated larvae restored the steady-state levels or even increased TRβ and TRβv mRNAs with respect to the untreated control. Overall, these results demonstrate that TRβ transcription is up-regulated by THs playing a major role during metamorphosis in Senegalese sole. |
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ISSN: | 0016-6480 1095-6840 |
DOI: | 10.1016/j.ygcen.2008.11.001 |