Retinoic acid receptors and muscle b-HLH proteins: partners in retinoid-induced myogenesis.

The results reported here indicate that retinoic acid (RA) induces growth arrest and differentiation only in MyoD-expressing muscle cells. Transient transfection assays reveal a functional interaction between MyoD, a key myogenic regulator and RA-receptors, principal mediators of RA actions. Interestingly, we demonstrate that RXR-MyoD-containing complexes are recruited at specific MyoD DNA-binding sites in muscle cells.

Functional specificity of the two retinoic acid receptor RAR and RXR families in myogenesis.

In C2 myoblasts, retinoic acid (RA) is an efficient inducer of both growth arrest and differentiation. These RA effects are mediated through at least two classes of retinoic acid receptors (RARs and RXRs), which belong to the nuclear receptor superfamily. To determine the role played by each RAR or RXR family in this model system, we have analysed the effects of RA in C2 myoblasts expressing a dominant negative RAR (dnRAR) or a dominant negative RXR (dnRXR).

Expression of the estrogen-related receptor 1 (ERR-1) orphan receptor during mouse development.

We studied the expression of the estrogen-related receptor 1 (ERR-1) during mouse embryonic development. ERR-1 is expressed at very early stages in ES cells and at E8.5 in the mesodermal cells of the visceral yolk sac.

RXR alpha is essential for mediating the all-trans retinoic acid-induced growth arrest of C2 myogenic cells.

In C2 muscle cells, retinoic acid (RA) induces growth arrest associated with terminal differentiation. These RA actions are presumed to be mediated through nuclear receptors (RARs and RXRs) that belong to the superfamily of ligand-dependent transcription factors. In this study, we have characterized a myogenic C2 subclone, that unlike parental cells, is resistant to growth inhibition and differentiation by RA.