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Avian MyoD and c-Jun Coordinately Induce Transcriptional Activity of the 3,5,3'-Triiodothyronine Nuclear Receptor c-ErbA1 in Proliferating Myoblasts

Unité d’Endocrinologie Cellulaire, Unité Mixte de Recherche Différenciation Cellulaire et Croissance (Institut National de la Recherche Agonomique, Université Montpellier II, Ecole Nationale Supèrieure d’Agronomie de Montpellier), Institut National de la Recherche Agronomique, 34060 Montpellier, France

Address all correspondence and requests for reprints to: G. Cabello, Unité d’Endocrinologie Cellulaire, Unité Mixte de Recherche Différenciation Cellulaire et Croissance, Institut National de la Recherche Agronomique (INRA), 2 place Viala, 34060 Montpellier Cedex 1, France. E-mail: cabello{at}ensam.inra.fr.

Although physical interactions with other receptors have been reported, heterodimeric complexes of T₃ nuclear receptors (TR) with retinoid X receptors (RXRs) are considered as major regulators of T₃ target gene expression. However, despite the potent T₃ influence in proliferating myoblasts, RXR isoforms are not expressed during proliferation, raising the question of the nature of the complex involved in TR transcriptional activity. We have previously established that c-Jun induces TR1 transcriptional activity in proliferating myoblasts not expressing RXR. This regulation is specific to the muscle lineage, suggesting the involvement of a muscle-specific factor. In this study, we found that MyoD expression in HeLa cells stimulates TR1 activity, an influence potentiated by c-Jun coexpression. Similarly, in the absence of RXR, MyoD or c-Jun overexpression in myoblasts induces TR1 transcriptional activity through a direct repeat 4 or an inverted palindrome 6 thyroid hormone response element. The highest rate of activity was recorded when c-Jun and MyoD were coexpressed. Using c-Jun-negative dominants, we established that MyoD influence on TR1 activity needs c-Jun functionality. Furthermore, we demonstrated that TR1 and MyoD physically interact in the hinge region of the receptor and the transactivation and basic helix loop helix domains of MyoD. RXR expression (spontaneously occurring at the onset of myoblast differentiation) in proliferating myoblasts abrogates these interactions. These data suggest that in the absence of RXR, TR1 transcriptional activity in myoblasts is mediated through a complex including MyoD and c-Jun.