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Fig. 6 | Genome Biology

Fig. 6

From: BORIS/CTCFL epigenetically reprograms clustered CTCF binding sites into alternative transcriptional start sites

Fig. 6

BORIS expression is associated with a significant increase in CTCF occupancy and a more open chromatin state around CTCF sites. a CTCF occupancy mapped in NIH3T3 + EV versus NIH3T3 + BORIS (clone#2) cells, depicted through a violin plot. b Scatter plot shows normalized read counts (log10) for CTCF occupancy at the combined set of CTCF binding sites in NIH3T3 + BORIS (clone#2) cells compared to NIH3T3 + EV cells. CTCF sites with increased or decreased occupancy by more than threefold are highlighted in red and green, respectively. c Heatmap illustrating CTCF (red) and BORIS (blue) occupancy at the 6521 CTCF sites from panel b (connected by red arrow). d Scatter plot of normalized read counts (log10) for ATAC-seq tag density at the combined set of ATAC-seq genomic sites mapped in both NIH3T3 + EV and NIH3T3 + BORIS (clone#2) cells. Genomic sites with increased or decreased occupancy by more than twofold are highlighted in red and green, respectively. e Heatmaps combining ATAC-seq (black) accessibility with CTCF, BORIS, H2A.Z, H3K4me3, and H3K27ac occupancy at genomic regions from panel d (connected by red and green arrows). Upper and lower panels display data for increased and decreased ATAC-seq sites, respectively. f Average plot of chromatin accessibility (ATAC-seq) at 4654 BORIS binding sites that gained H2A.Z occupancy in NIH3T3 + BORIS (blue) cells compared to NIH3T3 + EV cells (black). P-value calculated by the Kolmogorov–Smirnov test. g Genome browser view of two alternative intronic promoters in Snx31 and Hsf3 genes activated by BORIS (blue) binding to CTCF (red) sites in NIH3T3 + BORIS (clone#2) cells. Black arrows indicate increased chromatin accessibility (ATAC-seq, black) beyond CTCF and BORIS ChIP-seq peaks. Red arrows show alternative transcription initiated from a CTCF binding site with BORIS recruitment

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