Fig. 1.

miR-3906 silences different target genes at different muscle developmental stages. a At the early muscle development, Dkk3a interacts with its receptor Itgα6b, resulting in the phosphorylation of p38a and the formation of the Smad2/3a/4 complex, which in turn, activates the myf5 promoter activity. When myf5 is highly transcribed, the intronic miR-3906 suppresses the transcription of myf5 through silencing the Dkk3a [39, 41–43]. b At the late muscle development, miR-3906 starts transcription at its own promoter and switches to silence homer1b to control the homeostasis of intracellular calcium concentration ([Ca²⁺]_i) in fast muscle cells [40]. Either miR-3906-knockdown or homer-1b-overexpression causes the increase of Homer-1b protein, resulting in an enhanced level of [Ca²⁺]_i, which in turn, disrupts sarcomeric actin filament organization. In contrast, either miR-3906-overexpression or homer-1b-knockdown causes the decrease of Homer-1b, resulting in a reduced [Ca²⁺]_i and thus a defective muscle phenotype [40]