Fig. 1: Summary of datasets generated in this study and analysis of GCM2 binding in parathyroids.

a List of select epigenomics profiles generated in this study and, as an example, the CASR gene. b t-SNE projection of RNA-seq from eight parathyroid adenoma samples (orange, arrow) based on parathyroid-specific expressions along with RNA-seq samples from 53 tissues profiled in the GTEx project where each dot represents each individual sample and each color represents each tissue type. c Distributions of GCM2 binding mapped to chromatin states in parathyroids. The numbers positioned above the bars represent the ratios of observed numbers to expected numbers. P-values from a one-sided Fisher’s exact test. TssA, Active TSS; TssFlnk, Flanking TSS; TssFinkU, Flanking TSS Upstream; TssFlinkD, Flanking TSS Downstream; Tx, Strong transcription; TxWk, Weak transcription; EnhG1, Genic enhancer1; EnhG2, Genic enhancer2; EnhA1, Active Enhancer1; EnhA2, Active Enhancer2; EnhWk, Weak Enhancer; ZNF/Rpts, ZNF genes & repeats; Het, Heterochromatin; TssBiv, Bivalent/Poised TSS; EnhBiv, Bivalent Enhancer; ReprPC, Repressed PolyComb; ReprPCWk, Weak Repressed PolyComb. d Heatmap showing the patterns of histone modifications around GCM2 peaks (±3 kb). Each row corresponds to each GCM2 binding site. GCM2 binding sites at the TSS-proximal (top) or distal to the TSS (bottom). e Super-enhancers in parathyroids. Enhancers sorted by H3K27ac signal intensities with super-enhancers defined by strong H3K27ac signals (orange line). Known key parathyroid genes are annotated in black and several genes previously not known to be key in adult parathyroids are annotated in orange; these genes were all found to be GCM2 targets.