In pancreatic β-cells myosin 1b regulates glucose-stimulated insulin secretion by modulating an early step in insulin granule trafficking from the Golgi
Hiroshi Tokuo, Shigeru Komaba, Lynne M. Coluccio
Abstract
-Golgi network (TGN) marker TGN38, and insulin granules in the perinuclear region. Myo1b depletion by small interfering RNA in 832/13 cells reduced intracellular proinsulin and insulin content and glucose-stimulated insulin secretion (GSIS) and led to the accumulation of (pro)insulin secretory granules (SGs) at the TGN. Using an in situ fluorescent pulse-chase strategy to track nascent proinsulin, Myo1b depletion in insulinoma cells reduced the number of (pro)insulin-containing SGs budding from the TGN. The studies indicate for the first time that in pancreatic β-cells Myo1b controls GSIS at least in part by mediating an early stage in insulin granule trafficking from the TGN.
Topics & Concepts
ProinsulinInsulinBiologyCell biologyInternal medicineGolgi apparatusEndocrinologyGranule (geology)ExocytosisSecretionEndoplasmic reticulumPaleontologyMedicinePancreatic function and diabetesMetabolism, Diabetes, and CancerCellular transport and secretion