Murine ES cells require leukemia inhibitory factor (LIF) signaling, which leads to phosphorylation and nuclear localization of the transcription factor STAT3 (Matsuda et al., 1999; Niwa et al., 1998). The genome-wide binding sites of STAT3 overlap extensively with Brg1 occupancy (Ho et al., 2009a), and the transcriptional changes caused by LIF withdrawal and acute Brg1 deletion are highly similar (Ho et al., 2011). This is in contrast to Oct4 (Loh et al., 2006; Masui et al., 2007) and Sox2 (Shao et al., 1999) whose targets also overlap with Brg1 binding sites but do not show consistent transcriptional co-regulation. Although there is no detectable physical interaction between STAT3 and Brg1, Brg1 knockout abolishes STAT3 binding at over 80% of sites; these sites become more resistant to DNase I digestion (Ho et al., 2011) indicative of a more ‘closed’ chromatin state (Dorschner et al., 2004). Creating accessibility at genomic sites may be a key function of the esBAF complex, and 80% of BRG1 target sites in ES cells are indeed DNase I hypersensitive (Schnetz et al., 2010).
