In this study, we sought to assess the role of two SWI/SNF BAF subunits and the catalytic subunit BRG1 in skeletal muscle terminal differentiation. Indeed, previous works were mainly focusing on the role of the catalytic subunits in SCH727965 differentiation programs, showing for example that BRG1 is actively involved in the expression of early and late muscle genes. BAFs are mainly considered as structural components of SWI/SNF complexes. However, recent papers showed that these subunits play important roles in a wide range of differentiation programs. For example, BAF60c plays an important role in muscle differentiation in a twostep model. First, it mediates the initial recognition of the myogenin promoter by MyoD in myoblasts and, following its phosphorylation by p38a kinase, recruits the SWI/SNF complex. In our study, we used siRNA-mediated downregulation of BRG1, BAF47 or BAF53a and analyzed the consequences on muscle differentiation and gene expression. Knockdown of BAF47, BAF53a or BRG1 impairs ex vivo myogenic differentiation of myoblasts. BAF53a-depleted cells exhibit almost standard levels of Myogenin, MCK and MHC since the observed decrease is not statistically significative. While in BAF47- or BRG1-depleted myoblasts, expression of muscle markers is largely decreased or even abolished. These results suggest different time-scale requirements for SWI/SNF subunits during differentiation. BAF53a being required in later steps for cell fusion but not so necessary for the appropriate program of early gene regulation, while BAF47 and BRG1 are required at early differentiation steps. Several studies reported the role of HDACs in muscle differentiation. HDACs are frequently incorporated in larger protein complexes mainly, involved in transcription repression. Some of these repressor complexes, such as N-CoR and mSin3A/HDAC, also include SWI/SNF subunits and other co-repressor factors. For example, it has been reported the presence of SWI/SNF members in the N-CoR-1 complex including BRG1, BAF170, BAF155, BAF47 and the co-repressor KAP1. We have performed interaction experiments and we were able to co-precipitate BRG1, BAF47 and BAF53a from proliferating myoblasts, as well as HDAC 1–3 and KAP1, which are specific of the N-CoR-1 complex. Interestingly, we found a weaker association of BAF47 with SWI/SNF subunits in differentiating as compared to proliferating myoblasts, while KAP1/BAF47 interactions are more stable in differentiating and proliferating myoblasts. In any condition of IP, we also coprecipitate MyoD. Participation of BRG1 and BAF47 to SWI/ SNF and N-CoR complexes was further assessed by complex fractionation on glycerol gradient. Comparing proliferating and differentiating myoblasts, we observed an increase of BAF47 in the fractions containing KAP1 and HDACs upon differentiation. Interactions between MyoD and SWI/SNF complexes as well as with N-CoR factor have been described, consistent with MyoD detection in nuclear extract fractions overlapping with BRG1 but also KAP1 distribution. Interaction of BRG1 and BAF47 with HDACs and KAP1 might be required for proper repression of transcription.