In neural progenitors, REST-mediated repression of miR-9* and miR-124 maintains BAF53a expression (Yoo et al., 2009). Forced expression of the miRNAs in Nestin+ neural progenitors leads to loss of BAF53a and impaired proliferation, consistent with the requirement for the BAF53a subunit in progenitor cell division (Lessard et al., 2007). On the other hand, REST is repressed in postmitotic neurons by the unliganded retinoic acid receptor (RAR) repressor complex (Ballas et al., 2005); this allows miR-9* and miR-124 to be expressed and as a result, BAF53a is targeted for repression by the miRNAs (Yoo et al., 2009). Mutating the miRNA binding sites on the BAF53a 3′ UTR leads to persistent BAF53a expression and reciprocal downregulation of BAF53b in β-Tubulin-III+ neurons, indicating that BAF53a antagonizes BAF53b gene activation. Prolonged expression of npBAF subunits, including SS18, is inhibitory to dendritogenesis, albeit being insufficient to reactivate cell cycle in postmitotic neurons (Staahl et al., 2013; Yoo et al., 2009). The SS18 gene also contains putative miR-9* and miR-124 binding sites, but it is unclear whether the same regulatory mechanism governs the switch from SS18 to CREST at this subunit position.
