Identifying the genomic regions where ASCL1 and mSWI/SNF remodelers are both required to regulate chromatin accessibility during neural differentiation [ATAC-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 performed ATACseq in WT, ASCL1 KO, and BRM014-treated cells at DIV24, when ASCL1 expression is highest during neural differentiation. Overall design: We performed differential accessibility analysis between WT and ASCL1 KO cells to identify the sites where ASCL1 regulates chromatin accessibility. We then investigated the accessibility level at those sites when cells were treated with BRM014 inhibitor and thus identified the regions where the ASCL1-mSWI/SNF interaction is required to shape the accessibility landscape.