of dicer results in decreased miRNA expression and defects in neuronal cell differentiation and survival (Kanellopoulou et al., 2005; Murchison et al., 2005; Schaefer et al., 2007). These phenotypes could be rescued by re-expression of the gene (Kanellopoulou et al., 2005), highlighting the importance for Dicer and the smRNAs species processed by this endoribonuclease in neuronal development and function. More recently, conditional deletion of Dicer established that miRNAs expressed during neurogenesis play a role in the maintenance of neural progenitor cells, with disruption in this action contributing to defects in neuronal migration and subsequently in cortical lamination (De Pietri Tonelli et al., 2008; Kawase-Koga et al., 2009; Clovis et al., 2012).
