Extended Data Fig. 5: TE-encoded regulatory elements in Setdb1 KO LLC and B16 cells.
From: Epigenetic silencing by SETDB1 suppresses tumour intrinsic immunogenicity

a, Proportion of chromatin accessible sites (ATAC-seq) gained in Setdb1 KO LLC or B16 cells that are located within (red) or outside (grey) SETDB1 domains. b, Proportion of ATAC-seq sites gained in Setdb1 KO LLC or B16 cells that coincide with promoters (light grey), distal TEs (red), or other promoter-distal sites (dark grey). Statistics by permutation testing. c, Proportion of gained ATAC-seq sites at distal TEs in Setdb1 KO B16 cells that also gain H3K27 acetylation and resemble active enhancers. d, Coordinate gain of chromatin accessibility and H3K27 acetylation at an example TE-site in Setdb1 KO B16 cells. e, Activation of genes near (<50 kb) gained ATAC-seq sites at distal TEs in Setdb1 KO LLC or B16 cells compared to control genes. Statistics by permutation testing. f–g, Flow cytometry in control and Setdb1 KO cells showing gating strategy (f), cell-surface expression (g) (y-axis, median fluorescence intensity (MFI)) for ULBP1 and RAET1 ligands in LLC (left), and MHCI expression in LLC and B16 (right) with or without induction with IFNγ (10 ng ml−1, 24 h). Data are mean ± s.e.m. and reflect 2 independent experiments with 4 biological replicates. Statistics by two-sided Student’s t-test. *P < 0.05; **P < 0.01.