Fig. 4

RA treatment leads to increased chromatin binding of its receptor RARαa. (A) Differential analysis of RARαa chromatin binding by ChIP-seq between atRA treated and control embryos at 80% of epiboly stage (n = 2 biological replicates per stage and condition). The log2P-value versus the log2 fold-change of ChIP-seq signal are plotted. Regions showing statistically significant differential binding (adjusted P-value < 0.05) are highlighted in blue (increased) or red (decreased). The total number of differential peaks is shown inside the box. (B) Violin plots showing the distribution of log2 fold-change of expression (RNA-seq) all DEGs and those associated with increased or decreased chromatin binding of RARαa. (C) Genome tracks of RARαa ChIP-seq, ATAC-seq and RNA-seq at 80% of epiboly stage showing signal intensities in the nr2f5 locus. The Genes track represents ENSEMBL annotated genes. (D) Heatmaps of the 1275 ATAC-seq peaks with increased accessibility in atRA treated embryos at 80% of epiboly stage, separating those overlapping (n = 376) or not (n = 880) RARαa peaks. Average profiles of both groups are shown on top. (E) Motif enrichment analysis of the peaks with increased accessibility and RARαa binding or without RARαa. The top-3 motifs have been selected for each stage. (F) Zebrafish wildtype expression terms enriched for the genes associated with increased ATAC-seq peaks and RARαa binding. No enriched GO terms were found for the genes associated with increased ATAC-seq peaks but without RARαa binding