Fig. 3

RBM22 controls the transcription termination of protein-coding genes. a Examples of POLR2G ChIP-seq and GRO-seq signals at two representative protein-coding genes (ARFGAP1 and FUS) in control, RBM22 knockdown HepG2 cells, showing the enhanced transcriptional readthrough in the absence of RBM22. b–c Heatmaps displaying the changes in POLR2G ChIP-seq (b) and GRO-seq (c) signals in a region from 2 kb upstream to 10 kb downstream of the TES of each protein-coding gene (N = 20,003) upon RBM22 knockdown in HepG2 cells. For the subtraction of heatmaps, the color bars depict the subtracted values of siRBM22 minus siControl. d RI distribution in control and RBM22 knockdown HepG2 cells, showing the enhanced transcriptional readthrough at many transcribed genes (N = 5626) upon RBM22 knockdown. The p value was determined using the Kolmogorov–Smirnov test. e Histogram showing the fold change (FC) of RI (GRO-seq) at protein-coding genes upon RBM22 knockdown in HepG2 cells. f TT-qPCR quantification of transcriptional readthrough at four representative protein-coding 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). g Venn diagram of DoGs discovered in the two individual conditions. h Length distribution of DoGs discovered in the three individual conditions. The percentage of DoGs of various lengths relative to the entire set of DoGs identified in individual conditions is shown on the y-axis. i Boxplot showing the GRO-seq signal at DoG regions in the two conditions