Fig. 4: Acetylated CRDs dysregulated in SCZ.

a, Proportional representation of SCZ-sensitive H3K27ac NeuN⁺ ΔCRDs stratified by hypo-acetylation (blue), hyper-acetylation (red) and not dysregulated (gray). Pie chart shows the proportion of dysregulated histone peaks ΔCRD_ΔPeaks inside ΔCRD. b, SCZ heritability coefficients shown separately for H3K27ac NeuN⁺ (blue) and H3K27ac Tissue (green), as indicated, by (1) ‘All CRD’: all peaks inside CRD (n = 114,123 and 143,092 peaks in CRD); (2) ‘ΔCRD’: dysregulated CRD (n = 28,866 and 15,787 peaks in ΔCRD and 3,507 and 1,673 peaks in ΔCRD_ΔPeaks); (3) ‘ΔCRD ↑ ’: hyper-acetylated with mean log₂FC (SCZ versus controls) > 0 (n = 14,710 and 7,770 peaks in ΔCRD ↑ and 1,825 and 873 peaks in ΔCRD ↑ _ΔPeaks); and (4) ‘ΔCRD ↓ ’: hypo-acetylated with mean log₂FC (SCZ versus controls) < 0 (n = 14,156 and 8,017 peaks in ΔCRD ↓ and 1,682 and 800 peaks in ΔCRD ↓ _ΔPeaks) classified on the x axis as ΔCRD for all peaks and ΔCRD_ΔPeaks for only dysregulated histone peaks. The overlap of peaks within the dysregulated CRDs in clusters with SCZ risk variants was assessed using LD score regression. ‘#’: significant for enrichment in LD score regression after FDR correction of multiple testing across all tests in the plot (Benjamini–Hochberg, multiple testing P < 0.05); ‘*’: nominally significant for enrichment (P < 0.05). Error bars show standard error in SCZ heritability from LD score regression. c, Representative example of a genomic region that spans ten peaks. Horizontal bars (blue, FDR 5%; gray, NS) mark peak-level analysis with a single differential peak (top row), hyper-acetylated CRD (middle row) and ΔCRD_ΔPeaks (bottom row).