Muscular dysgenesis (mdg) is a spontaneous mutation affecting the α1 subunit of the skeletal L‐type Ca2+ channel, mdg/mdg mice suffer from a skeletal muscle disease characterised by low levels of the slow Ca2+ current, lack of contractile activity, and immature organisation of skeletal muscle. Microinjections of a cDNA encoding α1 into mutant nyotubes restore excitation‐contraction coupling. We checked here that dysgenic myotubes transfected with expression vectors, including a full‐length α1 cDNA, also recover normal ultrastructural features. Transfection of α1 cDNA partially deleted on the 5' end leads to the recovery of a good structural organisation without any improvement in the mutant physiological phenotype. These results suggest that: (i) the proper expression of αl is required for the full muscle differentiation of muscular dysgenesis myotubes, and (ii) portions of the α1 molecule may be involved in the structural organisation of a muscle fiber, independent of its known functional properties.