Inability to Switch from ARID1A-BAF to ARID1B-BAF Impairs Exit from Pluripotency and Commitment towards Neural Crest Formation in ARID1B-Related Neurodevelopmental Disorders

ARID1B-BAF regulated exit from pluripotency and lineage commitment by attenuating thousands of enhancers and genes of the NANOG and SOX2 networks. In iPSCs, these enhancers were maintained active by ARID1A-containing BAF.