Skip to main content
. 2015 Feb 15;29(4):379–393. doi: 10.1101/gad.254425.114

Figure 5.

Figure 5.

The H3K9 methylation-binding activity of GLP was required for efficient H3K9me2 establishment during ESC differentiation at a genome-wide level. (A) Clustering of the 10-kb genomic windows according to their H3K9me2 levels for wild-type (WT) and GLP 3A cells with or without RA treatment. The fold enrichment values of three biological replicates were averaged, centered to the mean of rows, and normalized to standard deviation by rows (Z-score in A–C). (B) Clustering of the 10-kb genomic windows according to their H3K9me2 levels for all replicates in wild-type and GLP 3A cells with or without RA treatment. (C) Clustering of the 3307 10-kb genomic windows (shown in A) according to their H3K9me1 levels for wild-type and GLP 3A cells with or without RA treatment. The values are averages of three biological replicates. (D,E) Accumulative distribution of H3K9me2 (D) and H3K9me1 (E) fold changes between RA-treated cells and ESCs at genic regions. (F) Number of genes with significantly changed H3K9me2 in wild-type or GLP 3A cells after RA treatment. (G) MA plot of H3K9me2 fold changes against the average H3K9me2 fold enrichment. Red dots represent genes with significantly increased H3K9me2 levels after RA treatment in wild-type cells. (H) Box plot of H3K9me2 fold changes between ESCs and RA-treated cells at genes acquired by H3K9me2 (shown in G) in wild-type and GLP 3A cells. (I) H3K9me2 profile at genic regions of genes acquired by H3K9me2 (shown in G) in ESCs or RA-treated wild-type (left) and GLP 3A (right) cells. “Rep 1–3” represents the three biological repeats. Lengths of genes were normalized to 100 percentiles and extended 20% upstream of and downstream from the gene body, respectively.