Fig. 4

RBM22-mediated transcriptional control at snoRNA and snRNA genes. a Examples of POLR2G ChIP-seq and GRO-seq signal at two representative sno/snRNA genes (U3 and RNU1-60P) in control and RBM22 knockdown HepG2 cells, showing the enhanced transcriptional readthrough induced by RBM22 knockdown. b Metagene analysis showing the change in POLR2G ChIP-seq signal at independently transcribed snoRNA and snRNA genes (N = 25) upon RBM22 knockdown. c Metagene analysis showing the change in GRO-seq signal at independently transcribed snoRNA and snRNA genes (N = 25) upon RBM22 knockdown. d Histogram showing the fold change of RI value for sno/snRNA genes upon RBM22 knockdown, ranked according to RI value. Doughnut plot displaying the number of genes with significant RI change, determined by |log2FC|> 0.58 (n = 11). SnoRNA/snRNA genes occupied by POLR2G in the control condition, as defined by having a peak called MACS2 and not overlapped with transcribed genes were used (n = 17). e TT-qPCR quantification of transcriptional readthrough at three representative sno/snRNA genes before (without 5-Ph-IAA) or after (with 5-Ph-IAA) RBM22 degradation in mAID-RBM22 cells. The readthrough ratio in untreated cells (without 5-Ph-IAA) was set to 1. Error bars represent the SD. The p values are determined using the two-tailed unpaired t-test (*p ≤ 0.05; **p ≤ 0.01; ns, not significant)