Additional file 13: of Identification of the BRD1 interaction network and its impact on mental disorder risk

Integrative analysis of ChIP-seq and gene-expression data. In order to investigate the gene-regulatory potential of BRD1-S and BRD1-L, ChIPseq data were integrated with expression data. A window of +/– 200 kb from BRD1 binding was constructed, fragmented in 9 kb segments, and determined the number of DEGs having TSSs in these segments. As opposed to the 10 kb segment used in the main manuscript the 9 kb segments used here span across 0 on the x-axis. A, B The analysis was performed for DEGs identified after upregulating BRD1-S or BRD1-L or (C, D) downregulating endogenous BRD1. Significantly more up- or downregulated genes were identified in segments where BRD1-S or BRD1-L binds in close proximity to TSSs compared to all segments across the window (P <0.001, 1-sample Student’s t-test). E, F The analysis was also performed after upregulating BRD1-S or BRD1-L and using a narrow window of +/– 5 kb from BRD1 binding sites. In order to investigate the BRD1 gene-regulatory potential while considering all genes on the array (and not only DEGs), probes were segmented according to TSS distance from BRD1 binding site following calculation of the average fold change of all probes within windows +/– 10 kb and +/– 200 kb from BRD1binding sites. F, G These two analyses show the mean expression fold changes combined from several genes and their distance from either BRD1-S or BRD1-L binding on the genome. F The first analysis shows the mean probe fold change in segments of 400 probes and using a +/– 10 kb window. G The second analysis shows the mean probe fold change in segments of 500 probes and using a +/– 200 kb window. (PDF 753 kb)