ESCs are characterized by hyperdynamic chromatin, which is compacted when these cells exit from their pluripotent state and differentiate into cells of multiple lineages. In the self-renewing state, chromatin remodellers are required to prevent this chromatin compaction (CHD1) and to repress and refine the inappropriate expression of genes (esBAF and the TIP60-p400 complex) that would otherwise be allowed by the permissive chromatin landscape. Exit from this self-renewing state into a state that allows multilineage commitment involves global changes in chromatin configuration, such as the formation of heterochromatin and the silencing of pluripotency genes (BAF complexes and NURD complexes), and key signalling events (bone-morphogenetic-protein-mediated signalling pathway and NURF complexes). Not surprisingly, evidence is emerging that chromatin remodellers such as BAF complexes (by way of an unknown mechanism) are crucial for the reversal of development and the reactivation of pluripotency genes such as Oct4, which occurs during the nuclear reprogramming of a committed cell type back into an ESC-like state. The proteins known to be involved are listed, together with the chromatin-remodelling complex they are found in (CHD, orange; SWI/SNF, green; ISWI, yellow; and INO80, pink).
