During aging, the pancreatic endocrine islets undergo chronic inflammation, which is associated with a reduced capacity for self-renewal of the insulin-producing beta-cells in zebrafish.

A previously undescribed protein produced by certain resident intestinal bacteria induces zebrafish pancreatic beta cell expansion.

Pancreatic α and β cells have different cell autonomous signatures; this explains why α but not β cells can clear infections by potentially diabetogenic viruses.

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

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

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.

Compartmentalized oscillations of second messengers affect global cellular signaling.

Nanodomain clustering of cAMP effectors represents a novel mechanism of cAMP compartmentation within an oscillatory signaling circuit.

Electron cryo-microscopy has revealed the three-dimensional structure of a potassium channel that has a central role in regulating the release of insulin from the pancreas.

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.