Figure 5
(a) Proportions of differential islet ATAC-seq peaks of type 2 diabetic versus non-diabetic donors annotated to different genomic regions. (b) Bar graph of differential islet ATAC-seq peaks of type 2 diabetic versus non-diabetic donors that overlap with histone modifications. (c-d) Sequencing tracks of ATAC-seq peaks that are more prevalent in donors with type 2 diabetes (annotated to MIR1178) (c) or non-diabetics (annotated to PTPN9) (d). The ATAC-seq data have been normalized to take sequencing depth into account. (e) Disease related pathways based on enrichment of genes annotated to differential islet ATAC-seq peaks of type 2 diabetic versus non-diabetic donors. The same pathways were significant when analyzing genes annotated to the 1,044 peaks enriched in T2D versus non-diabetic donors (Padj = 0.0159, Padj = 0.0175, Padj = 0.324 and Padj = 0.0425, respectively). Padj are adjusted by FDR. (f) Enrichment of transcription factor recognition sequences in differential islet ATAC-seq peaks of type 2 diabetic versus non-diabetic donors based on HOMER17.
