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. 2022 Apr 15;13(4):353. doi: 10.1038/s41419-022-04767-z

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© The Author(s) 2022

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 9 — A Schematic outlining digital genomic transcription factor (TF) footprinting from ATAC-seq of ND and T2DM islet samples (SRP117935) [35]. Transcription factors (e.g., REV-ERBα) protect against Tn5 digestion, resulting in a local decrease in chromatin accessibility (‘footprint’). This enables for identification and differential analysis of transcription factor binding at regulatory motifs in non-diabetic (ND) versus Type 2 Diabetic (T2DM) islets using the Hmm-based IdeNtification of Transcription factor footprint framework (HINT) [36]. B Venn diagram highlighting the overlap of REV-ERBα footprints identified in promoter regions (±1 kb from TSS) from at least two ND and/or T2DM islet samples (n = 5 ND and n = 5 T2DM samples). C–E (left): Representative ND and T2DM REV-ERBα footprints uniquely observed in T2DM islets (top), uniquely in ND islets (middle), and common (bottom) in both ND and T2DM islets within promoter regions. The signal is normalized to the total read depth of each sample and is plotted ±35 bp from the REV-ERBα motif center. C–E (right): Enriched GO: Biological Process pathways annotated from T2DM unique (top), ND unique (middle), and common (bottom) REV-ERBα footprints in promoter regions. F Forrest plot illustrating results of the meta-analysis for genes annotated as REV-ERBα footprints (unique to T2DM) derived from 5 publicly available human islet microarray datasets comparing the transcriptome of non-diabetic and type 2 diabetic islets (GSE38642 [63], GSE 25724 [64], GSE20966 [65], GSE76894 [66], and GSE76895 [66]). Red arrows highlight common genetic regulators of autophagy and protein degradation in T2DM.