The chromatin accessibility change by PRC2 inactivation with or without IFNγ stimulation in human MPNST cancer cells. The chromatin accessibility change by PRC2 inactivation with or without IFNγ stimulation in human MPNST cancer cells

PRC2-isogenic human malignant peripheral nerve sheath tumor (MPNST) M3 cells were generated through CRISPR/Cas9-mediated knockout of the PRC2 core component, SUZ12. PRC2 loss led to not only significant increase, but also significant decrease of chromatin accessibility at 15,346 (16% of all ATAC peaks) and 20,099 genomic loci (21% of all ATAC peaks), respectively. PRC2 loss decreased the chromatin accessibility for IFNγ-responsive loci in M3 cells, resulting in dampened response to IFNγ stimulation. Overall design: PRC2-isogenic human MPNST M3 cells (sgCon, sgSUZ12) were treated with PBS or 10 ng/ml IFNγ stimulation for 24 hr, followed by chromatin accessibility profiling.