This transition is caused by the Da and AS-C genes, which are transcription factors with the basic helix-loop-helix (bHLH) domains.
The interaction between Da or AS-C proteins with Emc to form dimers renders them inactive as transcription factors.
It is the interplay between concentrations of Da, AS-C, and Emc proteins that determines whether or not a cell will become an SMC, and later on an SO.
As females have twice the amount of Sc as males, they can overcome this obstacle and express the Sxl gene.
[1] Early support for the role of emc came from the mouse Inhibitor of differentiation (Id) gene, which negatively regulates myogenesis by forming a heterodimer with the MyoD protein and therefore inhibiting its abilities as a transcription factor.