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. 2019 Oct 22;8:e51109. doi: 10.7554/eLife.51109

Figure 5. Association between cellular ICP4 binding and chromatin.

MRC5 cells were uninfected or infected with HSV-1 for 2 h. All data was aligned to the human genome (hg38) and normalized for sequencing depth. (A, C–D) ChIP-Seq data for ICP4, Pol II, H3, H3K4me3, H3K27acetyl, H3K9me3, and H3K27me3. (B) ATAC-Seq data. (A–B) Sequencing data centered + /- 1 kilobase from the TSS of cellular mRNAs. Data was stratified for ICP4 binding using K-means clustering. (C) Spearman correlation analysis, limited to cellular transcripts. (D) Intersection of MACS2 peaks, analyzed as number of intersecting peaks or Jaccard statistic.

Figure 5.

Figure 5—figure supplement 1. MRC5 cells were uninfected or infected with HSV-1 for 2 h, and ChIP-Seq for ICP4, Pol II, H3, H3K4me3, H3K27acetyl, H3K9me3, and H3K27me3 was performed.

Figure 5—figure supplement 1.

Data was aligned to the human genome (hg38) and normalized for sequencing depth.
Figure 5—figure supplement 2. MRC5 cells were infected with HSV-1 for 2 h, and ChIP-Seq for ICP4, Pol II, H3, H3K4me3, H3K27acetyl, H3K9me3, and H3K27me3 was performed.

Figure 5—figure supplement 2.

Data was aligned to the human genome (hg38). IP peaks consistent between biological duplicate experiments were determined using MACS2. ChIPSeeker assessment of bound regions for each set of IP peaks.