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. 2020 Dec 14;9:e55730. doi: 10.7554/eLife.55730

Figure 4. Cardiac ECs maintain open chromatin at CMF genes.

(A) Representative ATACSeq gene tracks for cardiomyocyte, fibroblast, or endothelial cell genes in isolated GFP+ (endothelial, in red) or GFP- (non-endothelial, in black) nuclei. (B) Genome-wide open chromatin at the transcriptional start sites (TSSs) of cardiomyocyte, stromal, or endothelial cell genes in GFP- (non-endothelial) and GFP+ (endothelial) nuclei. Note chromatin of cardiomyocyte genes (red) is as open in ECs (GFP+) as non-ECs (GFP-). (C) Comparison of accessibility in GFP- vs GFP+ nuclei at TSS peaks (+/- 250 bp) for EC genes (green), cardiomyocyte genes (red), and stromal genes (blue). Note again that chromatin of cardiomyocyte genes is as open in EC as non-EC nuclei. (D) Motif enrichment analysis of ATACSeq peaks unique to non-endothelial (GFP-) nuclei (top), unique to endothelial (GFP+) nuclei (bottom), and shared peaks (middle). Right panels: gene ontology (GO) analysis of genes within 2 kb of each peak set. Full statistics and GO annotations for peak regions shown in Supplementary file 3. Additional analyses shown in Figure 4—figure supplement 1.

Figure 4.

Figure 4—figure supplement 1. Differential accessibility at all peaks associated with CMF genes.

Figure 4—figure supplement 1.

(A) Comparative accessibility (Log2RPKM) of all peaks associated with CMF genes in the non-EC (GFP-) nuclei of NuTRAP hearts vs cardiac and lung endothelial cells (GFP+). All peaks highlighted in red are differentially accessible between GFP- and GFP+ nuclei from heart, as calculated by DiffBind (DESeq2). (B) Annotation of all cardiac endothelial cell peaks vs those that are differentially accessible between GFP- and GFP+. Differentially accessible regions are primarily in enhancer (intergenic and intronic) regions rather than transcriptional start sites. (C) Representative tracks of peaks with differential accessibility between GFP- and GFP+ nuclei from heart. As shown in (B), differential peaks are found in enhancer regions of CMF genes.