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Pathways that control cortical F-actin dynamics during secretion.

J M Trifaró·T Lejen·S D Rosé·T Dumitrescu Pene·N D Barkar·E P Seward
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Abstract

Chromaffin cells possess a mesh of filamentous actin underneath the plasma membrane which acts as a barrier to the chromaffin vesicles access to exocytotic sites. Disassembly of cortical F-actin in response to stimulation allows the movement of vesicles from the reserve pool to the release-ready vesicle pool and, therefore, to exocytotic sites. The dynamics of cortical F-actin is controlled by two mechanisms: a) stimulation-induced Ca2+ entry and scinderin activation and b) protein kinase C (PKC) activation and MARCKS phosphorylation as demonstrated here by experiments with recombinant proteins, antisense olygodeoxynucleotides and vector mediated transient expressions. Under physiological conditions (i.e., cholinergic receptor stimulation followed by Ca2+ entry), mechanism (a) is the most important for the control of cortical F-actin network whereas when Ca2+ is released from intracellular stores (i.e., histamine stimulation) cortical F-actin is regulated mainly by mechanism b.

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ActinsAmino Acid SequenceAnimalsCalciumCalcium-Binding ProteinsCerebral CortexEnzyme ActivationGelsolinGlucosidasesHumansIntracellular Signaling Peptides and ProteinsMembrane ProteinsMicrofilament ProteinsMolecular Sequence DataMyristoylated Alanine-Rich C Kinase SubstratePhosphoproteinsProtein Kinase CJournal ArticleResearch Support, Non-U.S. Gov'tReview

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J M Trifaró, T Lejen, S D Rosé, T Dumitrescu Pene, N D Barkar, E P Seward. 2002. Pathways that control cortical F-actin dynamics during secretion.. https://doi.org/10.1023/a%3A1021627800918

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