The specific configuration of subunits in esBAF is crucial for the ES cell state. Brm, the alternative ATPase subunit, is not found in esBAF and does not compensate for the absence of Brg1 (Bultman et al., 2000); moreover, Brm−/− mice are viable despite being slightly larger than normal (Reyes et al., 1998). Similarly, the esBAF component BAF155 and its homolog BAF170 do not have redundant roles in ES cells. Knockdown of BAF155 in ES cells causes defects similar to Brg1 knockdown, with decreased proliferation followed by loss of Oct4 and increased cell death (Ho et al., 2009b). This phenotype is rescued by overexpressing BAF155 but not BAF170. In addition, BAF170-expressing ES cells do not contribute efficiently to teratoma formation in vivo, indicating that forced assembly of BAF170-containing BAF complexes in ES cells is detrimental to pluripotency.
