However, it has also been reported that apamin inhibits calcium current in neonatal chick and fetal cells. These reported differences of apamin on calcium current may reflect maturationdependent differences in channel subunit expression. We did not directly evaluate the effects of apamin on calcium current, but our experimental system is closest to that in the recent report by Yu et al., suggesting that block of calcium current was unlikely to mediate the observed effects of apamin in the present study. However, other studies report that BAF47/INI1 is also implicated in differentiation of hepatocytes and adipocytes. Among other BAF subunits, BAF53/ARP4/ACTL6 is a nuclear Actin Related Protein play different roles. Indeed, its interaction with the core SWI/SNF complex is required for the maximal ATPase activity of BRG1 and for the association of the SWI/SNF complex with chromatin. Two distinct BAF53 genes have been described, BAF53a and BAF53b. This subunit is an essential regulator of adult stem cell function. BAF53 is involved in self renewal of progenitor and stem cells, like long-term HSC, myeloid progenitor cell, neural stem and progenitor cells and epidermal progenitor cells. Several studies have shown the involvement of SWI/SNF complex in skeletal muscle terminal differentiation. There are functional interactions between different master myogenic bHLH transcription factors and many SWI/SNF subunits during myoblast-to-myotube transition. Indeed, dominant-negative forms of BRM or BRG1 inhibited muscle marker expression and terminal differentiation. In contrast, BAF57 has been shown to act as a partner of zinc Torin 1 fingercontaining factor Teashirt to repress MyoD-dependent myogenin expression and regulate skeletal muscle differentiation. In addition, BAF60c and MyoD interact on the regulatory elements of MyoD-target genes in myoblasts. Phosphorylation of BAF60c by p38a kinase induces SWI/SNF complex recruitment to muscle gene promoters through interaction with the BAF60c/MyoD complex and allows transcriptional activation of muscle target genes. Lack of BAF60c prevents myogenic programming. Although SWI/SNF complexes have been implicated in skeletal muscle terminal differentiation, the role of BAF47 in this process remained elusive. The aim of the present study is to unravel, in an ex vivo model of skeletal muscle terminal differentiation, specific roles of BAF47 compared to BRG1 and BAF53a, which roles have not been studied. Our data show that knockdown of one of these three subunits induced impairment in ex vivo skeletal muscle terminal differentiation. Most importantly, this impairment seems to involve more than their roles within the SWI/SNF complexes. Our results unravel crucial and specific roles for these subunits in the balance between proliferation and terminal differentiation in skeletal muscle. The SWI/SNF complex remodels chromatin structure, once recruited to gene promoters by transcription factors or histone modifications, through disruption of DNA-histone interactions to activate/repress gene expression. Skeletal muscle terminal differentiation is a two-step process starting with an irreversible cell cycle withdrawal.