the miRNAs alone were not sufficient to induce functional iN cells. However, the addition of the transcription factors NEUROD2, ASCL1, and MYT1L greatly increased the conversion efficiencies and led to the formation of iN cells from fetal and adult human fibroblasts with all the major functional properties of neurons, including synapse formation. Intriguingly, also this report underscored the essential role of bHLH transcription factors for generation of human iN cells. miR-9* and miR-124 are specifically expressed in post-mitotic neurons and were shown to repress the expression of SWI/SNF complex subunit Baf53a. When neural progenitor cells exit the cell cycle and differentiate into neurons, Baf53a is replaced by Baf53b and this switch is functionally relevant (Yoo et al., 2009). Therefore, one possibility was that the miRNAs facilitated reprogramming through promoting this BAF complex subunits switch. However, prolonging the expression of BAF53a did not abolish the conversion from fibroblasts to neurons and therefore downregulation of this miRNA target does not seem to be critical in this context (Yoo et al., 2011). Since Pang and colleagues showed iN cell induction by Neurod1, Ascl1, Myt1l, and Brn2, it appears that the miRNAs are able to replace the transcription factor Brn2 (Pang et al., 2011).
