Disrupting actin filaments enhances glucose-stimulated insulin secretion independent of the cortical actin cytoskeleton

Abstract

Just under the plasma membrane of most animal cells lies a dense meshwork of actin filaments called the cortical cytoskeleton. In insulin-secreting pancreatic {beta} cells, a longstanding model posits that the cortical actin layer primarily acts to restrict access of insulin granules to the plasma membrane. Here we test this model and find that stimulating {beta} cells with pro-secretory stimuli (glucose and/or KCl) has little impact on the cortical actin layer. Chemical perturbations of actin polymerization, by either disrupting or enhancing filamentation, dramatically enhances glucose-stimulated insulin secretion. We find that this enhancement does not correlate with the state of the cortical actin layer, suggesting filament disruptors act on insulin secretion independently of the cortical cytoskeleton.