Necdin mediates skeletal muscle regeneration by promoting myoblast survival and differentiation.

Regeneration of muscle fibers that are lost during pathological muscle degeneration or after injuries is sustained by the production of new myofibers. An important cell type involved in muscle regeneration is the satellite cell. Necdin is a protein expressed in satellite cell-derived myogenic precursors during perinatal growth.

Beta catenin-independent activation of MyoD in presomitic mesoderm requires PKC and depends on Pax3 transcriptional activity.

Early activation of myogenesis in the somite depends on signals from surrounding tissues. Canonical beta-catenin dependent Wnt signalling preferentially activates Myf5. We now show, in explant experiments with presomitic mesoderm, that the expression of another myogenic determination factor, MyoD, depends on non-canonical Wnt signalling, probably emanating from the dorsal ectoderm.

Msx2 and necdin combined activities are required for smooth muscle differentiation in mesoangioblast stem cells.

Little is known about the molecular mechanism underlying specification and differentiation of smooth muscle (SM), and this is, at least in part, because of the few cellular systems available to study the acquisition of a SM phenotype in vitro. Mesoangioblasts are vessel-derived stem cells that can be induced to differentiate into different cell types of the mesoderm, including SM. We performed a DNA microarray analysis of a mesoangioblast clone that spontaneously expresses an immature SM phenotype and compared it with a sister clone mainly composed of undifferentiated progenitor cells.