Fig. 1
From: Promoter G-quadruplex folding precedes transcription and is controlled by chromatin
Transcription is not necessary for G4 formation in promoters. a Experimental design overview. Black, data generated in this study; blue, published RNA-seq datasets. b Representative examples of G4 ChIP-seq genomic tracks in K562 cells for MYC and KRAS. From top to bottom tracks show G4 ChIP-seq signal (yellow), G4 ChIP-seq input control (yellow), ATAC-seq signal (green) and sequence motifs that can form G4s in vitro (defined as G4-seq sites, see ref [15]) on the forward (+ss) or reverse (−ss) strand (blue). The signal is quantified as count per million (CPM). c Box plot of Pol II ChIP-seq signal (log2CPM) at promoters (TSS ± 500 bp) in accessible chromatin (ATAC +) with an endogenous G4 (G4 ChIP +) or without a G4 (G4 ChIP−) but having sequence motifs that can fold into G4 structures in vitro (G4-seq). Wilcoxon-test: p < 2.2 × 10− 16. d Graphical representation of G4 formation and transcriptional inhibition experiments. e Western blotting for Pol II Ser2-P and total Pol II from K562 cells treated with or without 100 μM DRB for 1 h. ß-actin provides the loading control. f Bland Altman (MA) plot showing the fold change in G4 ChIP-seq signal at promoters between DRB-treated versus DMSO-treated K562 cells. Statistically significant (p < 0.01) higher and lower signals are in red and blue, respectively; black dots indicate regions not changing. g Western blotting for Pol II Ser5-P and total Pol II for K562 cells treated with or without 10 μM triptolide (TPL) for 30 min or 2 h. ß-actin provides the loading control. h MA plot similar to panel F illustrating the fold change in G4 ChIP-seq signal at promoters between TPL-treated versus untreated K562 cells (p < 0.01)