ArticleMolecular biology of the cell2014
Cdc42 controls the dilation of the exocytotic fusion pore by regulating membrane tension.
Article in Molecular biology of the cell, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 72 citations in OpenAlex.
- Vesicle docking and fusion pore modulation by the neuronal calcium sensor Synaptotagmin-1.Biophysical journal · 2025Article
- Cellular mechanisms of hormone secretion in neuroendocrine tumors: what goes wrong?Frontiers in cell and developmental biology · 2025Review
- Vesicle docking and fusion pore modulation by the neuronal calcium sensor Synaptotagmin-1.bioRxiv : the preprint server for biology · 2024Article
- Research progress on the regulatory role of cell membrane surface tension in cell behavior.Heliyon · 2024Review
- Fusion pore dynamics of large secretory vesicles define a distinct mechanism of exocytosis.The Journal of cell biology · 2023Article
- Article
- Three membrane fusion pore families determine the pathway to pore dilation.Biophysical journal · 2023Article
- Probing mechanical interaction of immune receptors and cytoskeleton by membrane nanotube extraction.Scientific reports · 2023Article
- Understanding the interplay of membrane trafficking, cell surface mechanics, and stem cell differentiation.Seminars in cell & developmental biology · 2023Review
- High-speed imaging reveals the bimodal nature of dense core vesicle exocytosis.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Integration of Bulk and Single-Cell RNA-Seq Data to Construct a Prognostic Model of Membrane Tension-Related Genes for Colon Cancer.Vaccines · 2022Article
- Downregulation of CDC42 inhibits the proliferation and stemness of human trophoblast stem cell via EZRIN/YAP inactivation.Cell and tissue research · 2022Article
- The neuronal calcium sensor Synaptotagmin-1 and SNARE proteins cooperate to dilate fusion pores.eLife · 2021Article
- TRIM67 regulates exocytic mode and neuronal morphogenesis via SNAP47.Cell reports · 2021Article
- Review
- Fusion Pore Expansion and Contraction during Catecholamine Release from Endocrine Cells.Biophysical journal · 2020Article
- Actin and Myosin in Non-Neuronal Exocytosis.Cells · 2020Review
- SNARE-Mediated Exocytosis in Neuronal Development.Frontiers in molecular neuroscience · 2020Review
- Ubiquitin-Specific Protease 8 Mutant Corticotrope Adenomas Present Unique Secretory and Molecular Features and Shed Light on the Role of Ubiquitylation on ACTH Processing.Neuroendocrinology · 2020Article
- Cdc42 Couples T Cell Receptor Endocytosis to GRAF1-Mediated Tubular Invaginations of the Plasma Membrane.Cells · 2019Article
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Authors and funding
12 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Membrane fusion underlies multiple processes, including exocytosis of hormones and neurotransmitters. Membrane fusion starts with the formation of a narrow fusion pore. Radial expansion of this pore completes the process and allows fast release of secretory compounds, but this step remains poorly understood. Here we show that inhibiting the expression of the small GTPase Cdc42 or preventing its activation with a dominant negative Cdc42 construct in human neuroendocrine cells impaired the release process by compromising fusion pore enlargement. Consequently the mode of vesicle exocytosis was shifted from full-collapse fusion to kiss-and-run. Remarkably, Cdc42-knockdown cells showed reduced membrane tension, and the artificial increase of membrane tension restored fusion pore enlargement. Moreover, inhibiting the motor protein myosin II by blebbistatin decreased membrane tension, as well as fusion pore dilation. We conclude that membrane tension is the driving force for fusion pore dilation and that Cdc42 is a key regulator of this force.
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