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Pathways that control cortical F-actin dynamics during secretion.

J M Trifaró1, T Lejen, S D Rosé

  • 1Secretory Process Research Program, Department of Cellular and Molecular Medicine, Faculty of Medicine, University of Ottawa, Ontario, Canada K1H 8M5. jtrifaro@uottawa.ca

Neurochemical Research
|January 7, 2003
PubMed
Summary
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Cortical F-actin disassembly in chromaffin cells is crucial for vesicle release. Two mechanisms, calcium entry and protein kinase C (PKC) activation, control this actin network dynamics.

Area of Science:

  • Cell Biology
  • Neuroscience
  • Biochemistry

Background:

  • Chromaffin cells have a sub-plasma membrane filamentous actin (F-actin) mesh.
  • This F-actin mesh acts as a barrier, restricting chromaffin vesicle access to exocytotic sites.

Purpose of the Study:

  • To investigate the mechanisms controlling cortical F-actin dynamics in chromaffin cells.
  • To elucidate how F-actin disassembly facilitates chromaffin vesicle exocytosis.

Main Methods:

  • Experiments utilized recombinant proteins, antisense oligodeoxynucleotides, and vector-mediated transient expressions.
  • Investigated the roles of calcium (Ca2+) entry, scinderin, protein kinase C (PKC), and MARCKS phosphorylation.

Main Results:

Related Experiment Videos

  • Cortical F-actin disassembly allows vesicle movement to release-ready pools and exocytotic sites.
  • Two primary regulatory mechanisms identified: (a) Ca2+ entry/scinderin activation and (b) PKC activation/MARCKS phosphorylation.
  • Mechanism (a) dominates under physiological cholinergic stimulation with Ca2+ entry.
  • Mechanism (b) is primary when Ca2+ is released from intracellular stores (histamine stimulation).

    • Conclusions:

    • Cortical F-actin dynamics are tightly regulated by distinct mechanisms depending on the stimulation pathway.
    • Understanding these mechanisms is key to comprehending regulated exocytosis in chromaffin cells.