As described earlier, the SWI/SNF-like complex in ESCs, esBAF, has a functionally and biochemically distinct composition that is required for self-renewal and pluripotency28,29. High-resolution genome-wide ChIP–Seq studies showed that the esBAF complex is present at about one-quarter of all promoters in mouse ESCs, with the intensity of binding correlating positively with the expression level of a gene. The targets of the esBAF complex are enriched for genes that are expressed highly and selectively by ESCs, and these overlap extensively with the targets of the transcription factors OCT4, SOX2, Nanog, STAT3 and SMAD1, suggesting functional interplay between the esBAF complex and these pluripotency factors in regulating genes involved in maintaining ‘stemness’30,32. A small number of genes have been studied in ESCs cultured in the prolonged absence of BRG1 or BAF components, and the findings suggest that the esBAF complex maintains ESC fate simply by activating ‘ESC genes’ and repressing genes involved in differentiation29–31. However, a genome-wide analysis carried out after acute depletion of BRG1 points to the esBAF complex having additional, more complex, modes of action32. Reduction of esBAF levels by
