Global Epigenomic Analysis of Primary Human Pancreatic Islets Provides Insights into Type 2 Diabetes Susceptibility Loci

Abstract

(Cell Metabolism 12, 443–455; November 3, 2010) In the preparation of this article, we made two typographical errors that we wish to correct:(1)The right promoter (marked by the right red box) in Figure 3B is incorrectly labeled. The correct label is: “Annotated islet-active promoter.”(2)The second sentence of the third paragraph in the Discussion section is incorrect. The corrected sentence is: “Focusing on T2D, 4 of the 12 elements that function as enhancers in vitro (FTO, KCNQ1, TCF7L2, and WFS1 loci) harbor T2D-associated SNPs, including two (TCF7L2 and WFS1 loci) that exhibit significant allele-specific differences in activity. This correction does not affect the data or the conclusions of the paper, and we apologize for any confusion the errors may have caused. Global Epigenomic Analysis of Primary Human Pancreatic Islets Provides Insights into Type 2 Diabetes Susceptibility LociStitzel et al.Cell MetabolismNovember 03, 2010In BriefIdentifying cis-regulatory elements is important to understanding how human pancreatic islets modulate gene expression in physiologic or pathophysiologic (e.g., diabetic) conditions. We conducted genome-wide analysis of DNase I hypersensitive sites, histone H3 lysine methylation modifications (K4me1, K4me3, K79me2), and CCCTC factor (CTCF) binding in human islets. This identified ∼18,000 putative promoters (several hundred unannotated and islet-active). Surprisingly, active promoter modifications were absent at genes encoding islet-specific hormones, suggesting a distinct regulatory mechanism. Full-Text PDF Open Archive