Fig. 6

P-TEFb dynamics on chromatin coordinated regulated by RBM22 and inhibitory 7SK snRNP. a Examples of HEXIM1, CDK9, and SPT5 ChIP-seq signals at two representative protein-coding genes (SGTA and RPL13) in control or RBM22 knockdown HepG2 cells. b Heatmaps displaying the reduction in HEXIM1 ChIP-seq signal at protein-coding gene promoters upon RBM22 knockdown. For the subtraction of heatmaps, the color bars depict the subtracted values of siRBM22 minus siControl. c Metagene analysis showing the change in CDK9 ChIP-seq signal in the promoter-proximal regions of protein-coding genes in control or RBM22 knockdown HepG2 cells. d Boxplot analysis of HEXIM1 occupancy signal at gene promoters with different RBM22 binding signals. The 1068 genes with HEXIM1 binding at the promoter were equally divided into three groups based on RBM22 occupancy at gene promoters. e Co-IP assay examining the interaction between endogenous HEXIM1 and CDK9 in mAID-RBM22 cells with 5-Ph-IAA or DMSO treatment. f Distance distribution of CDK9 ChIP-seq peak summit relative to TSS and + 1 nucleosome dyads, determined by MNase-seq, showing the pause release of P-TEFb at chromatin level upon RBM22 knockdown. The y-axis represents the gene number of CDK9 accumulation at relative positions from summit to TSS in control and RBM22 knockdown cells. g CDK9 PRR distribution showing the stronger pause release of P-TEFb at protein-coding genes upon RBM22 knockdown. The p value was determined using the Kolmogorov–Smirnov test. h 2D density plot displaying the high correlation between CDK9 PRR and RNAPII PRR in control and RBM22 knockdown HepG2 cells. The yellow line box represents the gene with PRR values higher than the median, which were used to compare the PRR change for CDK9 and RNAPII before and after the RBM22 knockdown. The p-value was determined using the Fisher test