Pharmacological inhibition of bromodomain and extra-terminal proteins induces an NRF-2-mediated antiviral state that is subverted by SARS-CoV-2 infection
Fig 4
SARS-CoV-2 infection and JQ-1 treatment modulate the chromatin regulatory landscape.
(A) TSS plot depicting the density and distribution of accessible ATAC-seq peaks around transcription start sites within a window of -500 to 500 bp. (B) Analysis of the genomic features annotated to accessible ATAC-seq peaks in the chromatin. (C) Heatmap of differentially accessible ATAC-seq peaks scaled as z-score across rows. (D-G) Volcano plots showing relative log2 fold change (log2FC) and statistical significance [-log10 (p-value)] of differentially accessible ATAC-seq peaks in (D) DMSO-treated infected/DMSO-treated uninfected, (E) JQ-1-treated uninfected/DMSO-treated uninfected, (F) JQ-1-treated infected/DMSO-treated infected, and (G) JQ-1-treated infected/JQ-1-treated uninfected contrasts. Significantly (FDR of ≤0.05) regulated peaks are indicated. (H-K) TF motif enrichment of accessible ATAC-seq peaks in (H) DMSO-treated infected/DMSO-treated uninfected, (I) JQ-1-treated uninfected/DMSO-treated uninfected, (J) JQ-1-treated infected/DMSO-treated infected and (K) JQ-1-treated infected/JQ-1-treated uninfected contrasts. The TF motifs were identified using the DREME algorithm, where the height of the letters represents the frequency of each base in the motif.