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Endocrinology Vol. 140, No. 3 1356-1364
Copyright © 1999 by The Endocrine Society

ARTICLES

ROR{alpha} Augments Thyroid Hormone Receptor-Mediated Transcriptional Activation1

Noriyuki Koibuchi, Ying Liu2, Harumi Fukuda, Akira Takeshita, Paul M. Yen2 and William W. Chin

Division of Genetics, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts 02115

Address all correspondence and requests for reprints to: Noriyuki Koibuchi, M.D., Ph.D., Division of Genetics, Department of Medicine, Brigham and Women’s Hospital, 75 Francis Street, Thorn 1004, Boston, Massachusetts 02115. E-mail: koibuchi{at}rascal.med.harvard.edu

This study is designed to clarify the role of an orphan nuclear hormone receptor, ROR{alpha}, on thyroid hormone (TH) receptor (TR)-mediated transcription on a TH-response element (TRE). A transient transfection study using various TREs [i.e., F2 (chick lysozyme TRE), DR4 (direct repeat), and palindrome TRE] and TR and ROR{alpha}1 was performed. When ROR{alpha}1 and TR were cotransfected into CV1 cells, ROR{alpha}1 enhanced the transactivation by liganded-TR on all TREs tested without an effect on basal repression by unliganded TR. By electrophoretic mobility shift assay, on the other hand, although ROR{alpha} bound to all TREs tested as a monomer, no (or weak) TR and ROR{alpha}1 heterodimer formation was observed on various TREs except when a putative ROR-response element was present. The transactivation by ROR{alpha}1 on a ROR-response element, which does not contain a TRE, was not enhanced by TR. The effect of ROR{alpha}1 on the TREs is unique, because, whereas other nuclear hormone receptors (such as vitamin D receptor) may competitively bind to TRE to exert dominant negative function, ROR{alpha}1 augmented TR action. These results indicate that ROR{alpha}1 may modify the effect of liganded TR on TH-responsive genes. Because TR and ROR{alpha} are coexpressed in cerebellar Purkinje cells, and perinatal hypothyroid animals and ROR{alpha}-disrupted animals show similar abnormalities of this cell type, cross-talk between these two receptors may play a critical role in Purkinje cell differentiation.




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