a, ChIP–seq in differentiated CAD neurons was performed in replicate with two different antibodies against ACSS2. Correlation plot displays relative enrichment over corresponding MACS peaks (default parameters with input as control, 1,598 peaks). b, Correlation plot displays relative genome-wide ChIP–seq enrichment. c, UCSC Genome Browser views of ChIP–seq tracks show that, upon CAD neuron differentiation, increases in H4K5, H4K12, and H3K9 acetylation over the Nudt1 locus co-occur with ACSS2 enrichment (chr5: 140,326,845–140,339,655). d, UCSC Genome Browser view of indicated ChIP–seq tracks in undifferentiated CAD cells and differentiated CAD neurons over Tab2 locus (chr10: 7,875,000–8,004,000). e, Gene ontology enrichment analysis of the genes most proximate to ACSS2 peaks demonstrates that neuron-specific genes are enriched. f, Frequency of ACSS2 peaks (T antibody) located upstream of their target gene associated with histone acetylation. g, Frequency of ACSS2 peaks (CS antibody) located upstream of their target gene associated with histone acetylation. h, Table shows per cent direct overlap of ACSS2 peaks with H3K9ac, H4K5ac, and H4K12ac broad MACS peaks. i–k, Decile plots depict enrichment of H3K9ac (i), H4K5ac (j), and H4K12ac (k) over ranked deciles of ACSS2 peak enrichment (zeroes removed). l–n, Differentiation-induced co-enrichment of ACSS2 and acetyl broad peaks (MACS). Peak enrichment correlation indicated for H3K9ac (l), H4K5ac (m), and H4K12ac (n). o, Discovered de novo motifs for transcription factor binding sites predicted by HOMER from all ACSS2 ChIP–seq peaks called by MACS in differentiated CAD neurons. p, ChIP–seq enrichment of differentiation-induced genes as a group shows correlation with histone acetylation in differentiated CAD neurons.