Fig. 3: Osmotic shock rapidly and transiently remodels chromatin in vivo.
From: Osmotic disruption of chromatin induces Topoisomerase 2 activity at sites of transcriptional stress
A Average (pileup) of CC-seq-v2 Top2cc signals oriented by local gene transcription direction around all transcription-factor binding sites in untreated cells and at time points following osmotic shock. B Fold change in density of CC-seq-v2 Top2cc signals in 50 bp bins centred on nucleosomal DNA midpoints56, inferred linker DNA midpoints, or sequence-specific transcription factor binding sites (ssTFs), in untreated cells and at time points following osmotic shock. C Average (pileup) of CC-seq-v2 Top2cc signals in a 2 kb region centred on 67548 nucleosome midpoints, in untreated cells and at time points following osmotic shock. Signals were smoothed with a 100 bp sliding Hann window. D Zoom into (C): region −1 to −0.5 kb relative to nucleosome midpoints, showing transient lengthening of the inter-peak distance induced by osmotic shock. E The mean interpeak distance (inferred as the inter-nucleosomal distance) in the average (pileup) of CC-seq-v2 Top2cc signals over a 2 kb region centred on 67548 nucleosome midpoints. F Pearson correlation between fold change in MNase-seq and CC-seq-v2 Top2cc signals at each time point following osmotic shock. Source data are provided as a Source Data file.
