The switching of npBAF subunits with nBAF subunits at mitotic exit is mediated by a triple-negative genetic circuitry involving non-coding micro-RNAs (miRNAs) (Figure 1) (Yoo et al., 2009). miRNAs achieve repression of their target genes by binding to transcripts and inhibiting translation or causing mRNA degradation (Lewis et al., 2005). The 3′ untranslated region (UTR) of BAF53a contains binding sites for miR-9* and miR-124, two neurogenic miRNAs which are abundant in neural tissue (Krichevsky et al., 2006; Lagos-Quintana et al., 2002; Cao et al., 2007; Makeyev et al., 2007; Visvanathan et al., 2007). The miRNAs are in turn subject to regulation by REST (Conaco et al., 2006), the transcriptional repressor which prevents neuronal gene expression in non-neuronal cells by binding to repressive element 1 (RE-1) on target genes and recruiting other repressors including CoREST and mSin3A (Grimes et al., 2000; Lunyak et al., 2002; Ballas et al., 2005; Chen et al., 1998; Chong et al., 1995).
