Fig. 6
From: Defective transcription elongation in a subset of cancers confers immunotherapy resistance
Chronic inhibition of TE recapitulates TEdeff. a Immunoblots of indicated histone and RNAP II marks in B16/F10 cells treated with flavopiridol for 72 h or 1 week. b Heatmap of the differentially expressed genes (i.e. P < 0.05) in chronic (1 week) flavopiridol-treated B16/F10 cells (log2 row normalized). c Expression change in TEdeff vs. TEprof cancer tissues (left), and genomic lengths (middle), of repressed and over-expressed genes in flavopiridol-treated cells, right) Expression change of Class I and Class II genes in flavopiridol-treated cells. d Calculation of the traveling RNAP II ratio from total RNAP II ChIP-seq data, which is defined as the ratio of occupancy of RNAP II along the gene bodies to that around the TSS. e Genome-wide comparison of RNAP II traveling ratio in the control and chronic flavopiridol-treated B16F10 cells. Each point depicts a gene, and Class I and II genes are colored accordingly. f Log fold change in RNAP II occupancy in the promoter and gene body regions in chronic flavopiridol-treated cells over control in Class I and II genes. g Spearman’s rank correlation of gene body RNAP II occupancy with overall polyA + mRNA expression (based on RNAseq data from b) in the respective genes in the parental and flavopiridol-treated B16F10 cells. h qPCR-based quantitation of expression of the indicated Jak1 exons in the parental and flavopiridol-treated B16F10 cells with and without 2 h stimulation with IFNγ. Error bars reflect s.d. of duplicate measurements. Statistical significance of difference is coded: (.): P < 0.1, (*): P < 0.05 by T-test. Boxplots: middle line: median, boxed areas extend from the first to third quartile; whiskers show 1.5x inter-quartile range from the first (bottom) or third (top) quartile
