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. Author manuscript; available in PMC: 2023 Jan 1.
Published in final edited form as: J Immunol. 2021 Dec 3;208(1):143–154. doi: 10.4049/jimmunol.2100923

Figure 5.

Figure 5.

DIVACs induce polymerase stalling A. ChIP-seq analysis of the RPB1, Spt5, S5P-CTD, and S2P-CTD of the genome-integrated Ri GFP2 (upper tracks) and Ri GFP2 2–3 (lower tracks) reporters and their surrounding region in DT40 cells as indicated.

B. The regions for the promoters (TSS +/−500 bp) and the bodies (TSS +1,000 bp to TTS) of genes analyzed in C.

C. Ratios of ChIP-seq signal (rpkm) in DT40 and Ramos cells with and without a DIVAC in the regions indicated in B. The ratios at the GFP transcription unit (green bars) were compared to the ratios of 500 most highly expressed genes (other genes, gray bars). The fold change at the GFP compared to other genes in the gene body is indicated in parentheses. The data are mean + SD.

D. ChIP-seq analysis of the RPB1, Spt5, and S5P-CTD of the GFP7 (upper tracks, no DIVAC) and SD2 GFP2 (lower tracks) reporters in the Ramos cells as indicated. A gap has been inserted in the tracks of reporters without a DIVAC after the alignment.