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

Alexander J. Polino, Xue Wen Ng, Rebecca Rooks, David W. Piston

Research output: Contribution to journalArticlepeer-review

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 β cells, a long-standing 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 β 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 enhance glucose-stimulated insulin secretion. Using scanning electron microscopy, we directly visualize the cortical cytoskeleton, allowing us to validate the effect of these filament-disrupting chemicals. We find the state of the cortical actin layer does not correlate with levels of insulin secretion, suggesting filament disruptors act on insulin secretion independently of the cortical cytoskeleton.

Original languageEnglish
Article number105334
JournalJournal of Biological Chemistry
Volume299
Issue number11
DOIs
StatePublished - Nov 2023

Keywords

  • F-actin
  • beta cell
  • cell cortex
  • depolymerization
  • hormone secretion
  • islet of Langerhans
  • pancreatic islet
  • polymerization

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