ArticlePloS one2013
Dynamin-2 regulates fusion pore expansion and quantal release through a mechanism that involves actin dynamics in neuroendocrine chromaffin cells.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed.
- Isolation and Purification of Chromaffin Granules from Adrenal Glands and Cultured Neuroendocrine Cells.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Gain-of-Function Dynamin-2 Mutations Linked to Centronuclear Myopathy Impair CaInternational journal of molecular sciences · 2022Article
- How filopodia respond to calcium in the absence of a calcium-binding structural protein: non-channel functions of TRP.Cell communication and signaling : CCS · 2022Article
- A review of Dynamin 2 involvement in cancers highlights a promising therapeutic target.Journal of experimental & clinical cancer research : CR · 2021Review
- Dynamin controls neuropeptide secretion by organizing dense-core vesicle fusion sites.Science advances · 2021Article
- Dynamin-2 R465W mutation induces long range perturbation in highly ordered oligomeric structures.Scientific reports · 2020Article
- Fusion Pore Expansion and Contraction during Catecholamine Release from Endocrine Cells.Biophysical journal · 2020Article
- SNARE-Mediated Exocytosis in Neuronal Development.Frontiers in molecular neuroscience · 2020Review
- Chromaffin Cells of the Adrenal Medulla: Physiology, Pharmacology, and Disease.Comprehensive Physiology · 2019Article
- Mechanistic study of PpIX accumulation using the JFCR39 cell panel revealed a role for dynamin 2-mediated exocytosis.Scientific reports · 2019Article
- Dynamin 1 Restrains Vesicular Release to a Subquantal Mode In Mammalian Adrenal Chromaffin Cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Local protein dynamics during microvesicle exocytosis in neuroendocrine cells.Molecular biology of the cell · 2018Article
- Actin dynamics at focal adhesions: a common endpoint and putative therapeutic target for proteinuric kidney diseases.Kidney international · 2018Review
- How does the stimulus define exocytosis in adrenal chromaffin cells?Pflugers Archiv : European journal of physiology · 2018Review
- RCAN1 Knockdown Reverts Defects in the Number of Calcium-Induced Exocytotic Events in a Cellular Model of Down Syndrome.Frontiers in cellular neuroscience · 2018Article
- Chemistry in a vesicle.The Journal of general physiology · 2017Article
- Dynamin-2 mutations linked to Centronuclear Myopathy impair actin-dependent trafficking in muscle cells.Scientific reports · 2017Article
- Fusion pores and their control of neurotransmitter and hormone release.The Journal of general physiology · 2017Review
- Dynamin-2 Stabilizes the HIV-1 Fusion Pore with a Low Oligomeric State.Cell reports · 2017Article
- The F-Actin Binding Protein Cortactin Regulates the Dynamics of the Exocytotic Fusion Pore through its SH3 Domain.Frontiers in cellular neuroscience · 2017Article
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Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Over the past years, dynamin has been implicated in tuning the amount and nature of transmitter released during exocytosis. However, the mechanism involved remains poorly understood. Here, using bovine adrenal chromaffin cells, we investigated whether this mechanism rely on dynamin's ability to remodel actin cytoskeleton. According to this idea, inhibition of dynamin GTPase activity suppressed the calcium-dependent de novo cortical actin and altered the cortical actin network. Similarly, expression of a small interfering RNA directed against dynamin-2, an isoform highly expressed in chromaffin cells, changed the cortical actin network pattern. Disruption of dynamin-2 function, as well as the pharmacological inhibition of actin polymerization with cytochalasine-D, slowed down fusion pore expansion and increased the quantal size of individual exocytotic events. The effects of cytochalasine-D and dynamin-2 disruption were not additive indicating that dynamin-2 and F-actin regulate the late steps of exocytosis by a common mechanism. Together our data support a model in which dynamin-2 directs actin polymerization at the exocytosis site where both, in concert, adjust the hormone quantal release to efficiently respond to physiological demands.
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