Journal
CELL SYSTEMS
Volume 7, Issue 3, Pages 310-+Publisher
CELL PRESS
DOI: 10.1016/j.cels.2018.07.007
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Funding
- JDRF [3-2012-263, 3-APF-2016-172-A-N]
- NIH [P50-HG007735, P50HG00773501]
- NIH Beta Cell Biology Consortium [UO1DK089532]
- NIH Human Islet Research Network [UC4DK104211, UC4DK1165252]
- Islet Research Core of the Stanford Diabetes Research Center [P30 DK116074-01]
- Howard Hughes Medical Institute
- Helmsley Charitable Trust
- H.L. Snyder Foundation
- Elser Foundation
- Doolittle Trust
- JDRF
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Understanding the genomic logic that underlies cellular diversity and developmental potential in the human pancreas will accelerate the growth of cell replacement therapies and reveal genetic risk mechanisms in diabetes. Here, we identified and characterized thousands of chromatin regions governing cell-specific gene regulation in human pancreatic endocrine and exocrine lineages, including islet beta cells, alpha cells, duct, and acinar cells. Our findings have captured cellular ontogenies at the chromatin level, identified lineage-specific regulators potentially acting on these sites, and uncovered hallmarks of regulatory plasticity between cell types that suggest mechanisms to regenerate beta cells from pancreatic endocrine or exocrine cells. Our work shows that disease risk variants related to pancreas are significantly enriched in these regulatory regions and reveals previously unrecognized links between endocrine and exocrine pancreas in diabetes risk.
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