Calcineurin fine tunes the balance between proliferation and differentiation of Notch-responsive progenitors in the pancreatic ducts to enable beta cell regeneration in zebrafish.

A mouse model of maturity-onset diabetes of the young illuminates that overactive TALK-1 channels limit β-cell calcium influx through membrane potential hyperpolarization, which blunts insulin secretion and causes glucose intolerance.

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

Intercellular communication is critical for organ function, and the role of innervation in mediating this communication is of relevance to many fields, including developmental biology, neuroendocrinology, and disease pathophysiology.

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

A novel algorithm, consensus non-negative matrix factorization (cNMF), accurately identifies gene expression programs underlying cell-type identity and cellular activities from single-cell RNA-Seq data.

Mutations causing proinsulin misfolding trigger unfolded protein response and lead to impaired proliferation and reduced mTORC1 signalling of developing beta-cells in a patient-derived induced pluripotent stem cell disease model.

A novel mode of organ innervation, whereby neurons establish connections with their targets before migrating away, was revealed by live imaging of the developing zebrafish pancreas.