Inter-nucleosomal communication between histone modifications for nucleosome phasing
Fig 5
H2A.Z knockdown induced decrease of nucleosome free regions and nucleosome phasing at TSS regions.
(a) Nucleosome profiles around TSSs in control group and H2A.Z knockdown group. TSSs are decreasingly ranked by their H2A.Z levels (the sum of normalized H2A.Z signal within -2000 to +2000 bp) in control group. (b) Nucleosome free regions (NFRs) marked in red color for control and knockdown groups. (c-e) Length (c), depth (d), and size (e) of nucleosome free regions. The median and quartile are shown. P-value was calculated by one-tailed t-test. (f) H2A.Z knockdown induced increase of nucleosome signals around TSS versus control group. The differential nucleosome profiles between H2A.Z knockdown and control group were calculated by DANPOS with the setting of “quantile normalization”. (g) Increase of “on-site” nucleosome occupancy on TSSs. TSSs are increasingly ranked by their H2A.Z levels in control groups, and the increase of “on-site” nucleosomes is plotted to show the mean ± SEM values within each bin of 1000 TSSs. Spearman correlation was calculated between the difference of “on-site” nucleosome occupancy at TSSs (the sum of differential nucleosome signals within -90 to +20 bp around TSS) versus the H2A.Z level (the sum of H2A.Z normalized-signals within -2000 to +2000 bp around TSS) of the corresponding TSSs in control group. (h) Cross-group linear regression for H2A.Z levels versus the nucleosome Phasing Index of control sample. Adjusted R2 and p-values are labeled on the panels. (I) Comparison of nucleosome profiles between control and knockdown samples. Nucleosome profiles are aligned within -2000 to +2000 bp around TSSs in a 10 bp resolution. TSSs (>20000 TSSs having non-zero H2A.Z signals at “+1” nucleosomes) are decreasingly ranked by H2A.Z levels at “+1” nucleosomes, and evenly divided into 10 groups.