The first evidence that BAF complexes could repress transcription through long-range interactions came from studies of mouse T cells. Normal T-cell development in the thymus depends on BAF complexes, although it is unclear whether thymocytes also have a specialized BAF complex. During development, T-cell differentiation is coupled to the differential expression of two co-receptors of the T-cell antigen receptor: CD4 and CD8. The expression of Cd4 is developmentally repressed by a distant silencer located 2 kb from the transcription start site of Cd4, and deletion of this silencer results in de-repression of Cd4 at an early stage of development45. The silencer binds to BRG1, BAF57 and presumably the entire BAF complex, which subsequently recruits a transcription factor required for Cd4 silencing, RUNX1 (which mediates repression by an unknown mechanism)46. BRG1-deficient thymocytes prematurely express CD4 and fail to activate CD8 expression, resulting in arrested thymocyte development47. This mode of action is distinct from that of the yeast Swi/Snf complex, which in all cases investigated is recruited to promoters by transcription factors in order to activate transcription48. Surprisingly, in mice, BRG1 is
