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Volume 271, Number 36, Issue of September 6, 1996 pp. 21950-21955
©1996 by The American Society for Biochemistry and Molecular Biology, Inc.

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Thyroid Hormone Activation of Transcription Is Potentiated by Activators of cAMP-dependent Protein Kinase

(Received for publication, May 24, 1996)

Dale C. Leitman , Cláudia H. R. M. Costa ^§ , Hans Graf ^¶ , John D. Baxter ^§ and Ralff C. J. Ribeiro ^§

From the  Department of Obstetrics, Gynecology and Reproductive Sciences and the ^§ Metabolic Research Unit, University of California, San Francisco, California 94143-0540 and the ^¶ Department of Endocrinology, Federal University of Paraná, Curitiba, Paraná 80060-900, Brazil

We characterized the cross-talk between activators of protein kinase A (PKA) and thyroid hormone (T₃) in T₃ receptor (TR)-mediated transcription. U937 cells were cotransfected with a plasmid expressing the TR and a reporter plasmid containing a T₃ response element (TRE) oriented either as a direct repeat or as a palindrome upstream of the thymidine kinase promoter linked to the chloramphenicol acetyltransferase gene. T₃ activated transcription by 10-fold. T₃ response was potentiated 2.5-3-fold by activators of PKA, but an activator of protein kinase C or of guanylate kinase was ineffective. In the absence of T₃, activators of PKA had no effect on transcription. TR heterodimerization with the retinoid X receptor may facilitate T₃/PKA cross-talk because coexpression of the retinoid X receptor potentiated cross-talk. Synergy was not observed in JEG-3, F9, CV-1, HeLa, L929, and HTC cells, indicating that it may require cell-specific factors. Synergy required the DNA- and ligand-binding domains, but not the amino-terminal domain, indicating that T₃- and TRE-induced conformational changes on the TR are essential for cross-talk. PKA phosphorylated the TR in vitro, suggesting that, like other nuclear receptors, the TR is a target for PKA. These results imply that PKA cross-talks with T₃ at the level of the TRE-bound TR, enhancing its transcriptional activity in a cell-specific manner.

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