Fig. 2: Promoter architecture influences Top2 activity.
From: Osmotic disruption of chromatin induces Topoisomerase 2 activity at sites of transcriptional stress
A Average (pileup) of CC-seq-v2 Top2cc signals around TSSs (left), gene body midpoints (middle), and TTSs (right). Signals were smoothed with a 100 bp sliding Hann window. B Average (pileup) of CC-seq-v2 Top2cc signals around transcription start sites (TSS) within promoters classified previously28: those bound by SAGA, TUP and/or Mediator SWI-SNF (STM); general transcription factors only (TFO); unbound by all but the pre-initiation complex (UNB); or those of ribosomal protein genes (RP). Signals were smoothed with a 100 bp sliding Hann window. C, D Boxplots of CC-seq-v2 Top2cc signal density in nucleosome depleted/free regions (NDRs) in (i) untreated or (ii) osmotically shocked cells (C), or of transcription activity measured by RNA-seq (D), for STM, TFO, UNB and RP genes. In all boxplot panels, upper and lower box limit: third and first quartile; bar: median; upper and lower whisker: highest and lowest values within 1.5-fold of the interquartile range. Statistical test used: two-sided K-S. Asterisks indicate Bonferroni-adjusted P values < 4.19 × 10−4, with colours, when present, indicating the specific pairwise comparison being tested. ns, P ≥ 0.838. E, F Average (pileup) of G1-arrested CC-seq-v2 Top2cc signals oriented by local gene transcription direction around all transcription-factor binding sites (E), or stratified by the indicated transcription factor classes (F). Note of the four classes, Fkh1 is known to be unbound in G1 cells30,31. Source data are provided as a Source Data file.
