This conserved mechanism of neuronal differentiation is not only necessary but instructive for the neuronal fate, allowing reprogramming from an unrelated lineage to postmitotic induced neurons (iNs) (Yoo et al., 2011). Expressing miR-9* and miR-124 in fibroblasts induces a cell fate conversion to functional neurons. The miRNA-overexpressing fibroblasts exit the cell cycle within one week, and while the starting cells express BAF53a, the resulting iNs robustly express the nBAF-specific subunits, BAF53b, BAF45b/c and CREST (Yoo et al., 2011; Staahl et al., 2013), indicating that the nBAF complex is operational. The efficiency of conversion is enhanced when the neurogenic transcription factor NEUROD2 is expressed in combination with the miRNAs, demonstrating their functional synergy. Unlikely many other lineages which are specified by master transcription factors (Weintraub, 1993; Davis et al., 1987; Nutt et al., 1999), a master regulator transcription factor for the diverse neuronal fates has not yet emerged. Intriguingly, the two neurogenic miRNAs as well as the nBAF-specific subunits are found throughout the CNS and are exclusive to the neuronal lineage (Yoo et al., 2009; Wu et al., 2007). Given the
