Analysis of epigenome maps from human pancreatic progenitors and functional validation in zebrafish identify LAMA1 and CRB2 as type 2 diabetes risk-associated genes with roles in pancreatic development.

The regulation of beta cell induction requires combined hierarchical and combinatorial transcriptional networks.

The signaling requirements to decouple proliferation of pancreatic progenitors from differentiation were elucidated and employed for the reproducible expansion, under GMP-compliant conditions, of pancreatic progenitors derived from different human pluripotent stem cell lines.

Loss of YAP1/TAZ expression in the pancreatic endocrine compartment is not a passive consequence of endocrine specification, rather, Hippo pathway-mediated inhibition of YAP1/TAZ in endocrine progenitors is a prerequisite for endocrine specification and differentiation.

A novel high-throughput, whole organism chemical screening platform was used to identify existing drugs that increase pancreatic beta-cell mass in zebrafish, implicating unique roles for the NF-κB and serotonergic signaling pathways in regulating pancreatic biology.

A set of cell surface markers reconstruct human pancreatic differentiation and enable the segregation of pancreatic functions into specific populations.

Most regenerated cells after β-cell damage in zebrafish are Insulin+ Somatostatin+ bihormonal cells that are functional and able to restore glucose control.

Ribosome profiling and loss-of-function during human ESC pancreatic differentiation reveal abundant lncRNA translation and an essential role for translated LINC00261 in beta cell differentiation, likely through a trans-regulatory, microprotein-independent mechanism.

ECM-Itgb1 signaling and cell-cell adhesion are pivotal and coordinate together to regulate pancreatic islet aggregation, architecture, and functional maturation during development.

Combinations of transcription factors can convert pancreatic acinar cells into endocrine α-, β- and δ-cells in vivo.