Fig. 4: Chromatin remodeling at pluripotency enhancers is dysregulated in the patient cells. | Nature Communications

Fig. 4: Chromatin remodeling at pluripotency enhancers is dysregulated in the patient cells.

From: Inability to switch from ARID1A-BAF to ARID1B-BAF impairs exit from pluripotency and commitment towards neural crest formation in ARID1B-related neurodevelopmental disorders

Fig. 4: Chromatin remodeling at pluripotency enhancers is dysregulated in the patient cells.

a At CNCC day 5, 29,578 ATAC-seq peaks are shared between patient and control lines. In all, 5540 peaks are specific to the patients. 578 peaks are specific to the controls. b UCSC Genome Browser example of a patient-specific ATAC-seq peak. c UCSC Genome Browser example of a CONTROL-SPECIFIC ATAC-seq peak. d ARID1B ChIP-seq heatmaps (Four lines; CNCC Day 5) centered on the patient-specific ATAC-seq peaks; the UCSC screenshot shows ARID1B binding at a patient-specific ATAC-seq peak (chr10:129,590,000–129,595,000) in the control and patient lines at iPSC stage and at CNCC Day 5. e Spike-in normalized heatmaps of H3K27ac ChIP-seq time-course at the 5540 patient-specific ATAC-seq peaks (Control Line-1). f Spike-in normalized H3K27ac ChIP-seq average profiles centered on the patient-specific ATAC-seq regions (CNCC Day 5). Statistical significance was assessed with Wilcoxon’s Rank-Sum test (p < 2.2 × 10−16 in all the patient vs control comparisons). g Spike-in normalized heatmaps of H3K27ac ChIP-seq signal at Days 5, 7, and 9 at the 5540 patient-specific ATAC-seq peaks (Control Line-1, Patient 19, Patient 26). h Motif analysis at the patient-specific ATAC-seq regions revealed enrichment for the binding motif of multiple pluripotency factors. P values are calculated by Meme-ChIP as E values. The E value is the motif P value (computed by Fisher’s Exact Test) times the number of candidate motifs tested.

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