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The triiodothyronine nuclear receptor c‐ErbAα1 inhibits avian MyoD transcriptional activity in myoblasts
Author(s) -
Daury Laetitia,
Busson Muriel,
Casas François,
Cassar-Malek Isabelle,
Wrutniak-Cabello Chantal,
Cabello Gérard
Publication year - 2001
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(01)03063-0
Subject(s) - myod , triiodothyronine , myocyte , pitx2 , nuclear receptor , chemistry , microbiology and biotechnology , myogenesis , medicine , endocrinology , biology , transcription factor , biochemistry , thyroid , gene , homeobox
Thyroid hormone stimulates myoblast differentiation, through an inhibition of AP‐1 activity occurring at the onset of differentiation. In this study we found that the T3 nuclear receptor c‐ErbAα1 (T3Rα1) is involved in a mechanism preserving the duration of myoblast proliferation. Independently of the hormone presence, T3Rα1 represses avian MyoD transcriptional activity. Using several mutants of T3Rα1, we found that the hinge region plays a crucial role in the inhibition of MyoD activity. In particular, mutations of two small basic sequences included in α helices abrogate the T3Rα1/MyoD functional interaction. Similarly, the T3 receptor also represses myogenin transcriptional activity. Therefore, despite stimulating avian myoblast differentiation by a T3‐dependent pathway not involving myogenic factors, T3Rα1 contributes to maintain an optimal myoblast proliferation period by inhibiting MyoD and myogenin activity.