Identifying the genomic regions co-bound by ASCL1 and mSWI/SNF remodelers during neural differentiation [ChIP-seq]

We interfeered with the ASCL1-mSWI/SNF interaction: to abolish ASCL1 function, we knocked out ASCL1 in human iPSCs, while we used the BRM014 inhibitor to block the mSWI/SNF ATPase activity. We then performed ASCL1 ChIPseq in DIV24 WT and BRM014-treated neural cultures, and SMARCB1 ChIPseq in DIV24 WT and ASCL1 KO neural cultures, when ASCL1 expression is highest. Overall design: We first identified the ASCL1 and SMARCB1 binding sites in DIV24 WT cultures, and then overlaped them to identify the ASCL1-SMARCB1 co-bound genomic regions. By comparing the ASCL1 binding profile in WT versus BRM014-treated cell, as well as the SMARCB1 binding profile in WT versus ASCL1 KO cells at the ASCL1-SMARCB1 co-bound regions, we were able to investigate the recruitment dynamics between ASCL1 and mSWI/SNF remodellers.