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. 2017 Aug 16;36(19):2829–2843. doi: 10.15252/embj.201796717

Figure 2. Heterochromatin is more susceptible to UV‐induced DNA lesions.

Figure 2

  1. Top panel: Boxplots of DNA lesion abundance within 15 previously defined chromatin states in IMR90 cells (Roadmap Epigenomics Consortium et al, 2015). Middle quartiles are represented by boxes, top and bottom quartiles are represented by whiskers. Gene‐rich chromatin states are labeled with green text, and gene‐depleted states are labeled with red text. Results are shown as abundance of DNA lesions within individual chromatin states divided by whole‐genome median. Whole‐genome distribution is shown as white box and was determined by pooling DNA lesion abundances from each chromatin state. Statistical outliers are omitted. Flanking and transcriptional start site are abbreviated as Flank and TSS, respectively. Middle panel, mean [log2(fold change/genome fold change average)] of representative histone modifications and DNase I hypersensitivity (HS) for chromatin states. Bottom panel: Enrichment significance of genes and repetitive features, previously defined (ENCODE Project Consortium et al, 2012), within each chromatin state. DNA transposable element, long interspersed nuclear element, and short interspersed nuclear element are abbreviated as TE, LINE, and SINE, respectively. P‐values are based on a hypergeometric distribution (refer to Materials and Methods for details).
  2. DNA lesion abundance was calculated as in panel (A) after binning by TpT content. Error bars denote the 95% confidence interval of the mean after bootstrapping 1,000 times.
  3. Fold change (FC) of DNA lesions (IP/input) within 1‐Mb windows compared to histone modification abundance and replication timing (Repl. Tim.) in IMR90 cells previously identified (ENCODE Project Consortium et al, 2012; Roadmap Epigenomics Consortium et al, 2015). Scatter plots with Pearson's correlation (r), linear regression lines (blue), and standard error interval are shown (gray).
  4. Variance explained from Random Forest Regressions using 10‐fold cross‐correlation is shown for “Active” chromatin (H3K36me3, H3K9ac, H3K4me3, H3K9ac), “Silent” (H3K9me3, H3K9me1, H4K20me1, H3K27me3), “Core Chromatin” (H3K9me3, H3K27me3, H3K4me1, H3K4me3, H3K36me3), and “All Chromatin” (16 histone modifications) (Roadmap Epigenomics Consortium et al, 2015).