Granule Fusion Membrane
Granule Fusion Membrane - Related Videos
09:19
Analysis of SNARE-mediated Membrane Fusion Using an Enzymatic Cell Fusion Assay
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2012
We have developed a cell fusion assay that quantifies SNARE-mediated membrane fusion events by activated expression of β-galactosidase.
01:43
SNAREs and Membrane Fusion
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2023
Once a transport vesicle has recognized its target organelle, the vesicular membrane needs to fuse with the target membrane to unload the cargo. Transmembrane proteins called SNAREs present on organelle membranes and their vesicles, mediate vesicle fusion. SNAREs exist in pairs that symmetrically interact and catalyze the fusion of the lipid bilayers in vesicle and target organelle. v-SNARE in the vesicle membrane are single polypeptide chains that bind to a complementary t-SNARE, composed of 2...
01:26
Fusion of Secretory Vesicles with the Plasma Membrane
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2023
Proteins and neurotransmitters in secretory vesicles can be released from a cell upon vesicle docking, priming, and fusion with the plasma membrane. Vesicles are docked and primed in preparation for the quick exocytosis of their contents in response to a stimulus. The fusion process is mainly carried out by a SNAP Receptor or SNARE complex, consisting of synaptobrevin, syntaxin-1, and SNAP-25. In 1993, Jim Rothman proposed that the antiparallel pairing of vesicular and transmembrane SNAREs, or...
16:01
Investigating Mast Cell Secretory Granules; from Biosynthesis to Exocytosis
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Cited by 9 •
2015
The goal of the present protocol was to develop a method that will allow functional genomic analyses of mast cell secretion. The protocol is based on quantitative assessment of the release of a fluorescent reporter gene cotrasfected with the gene of interest and real time analyses of the secretory granule's morphology.
03:34
An In Vitro Technique to Visualize Exocytosis of Secretory Granules in Mast Cells
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2025
This video demonstrates a technique to visualize exocytosis in mast cells. The cells are incubated with FITC-dextran — a fluorescent reporter — which is taken up by cells inside secretory granules (SGs), where the acidic pH quenches its fluorescence. Upon stimulation of granule exocytosis, the medium's higher pH induces reporter fluorescence inside the fused SGs, which is visualized using a fluorescence microscope.
FAQs
Antigen-receptor signaling increases cytosolic calcium inside the immune cell. That calcium signal activates vesicle-priming and membrane-fusion machinery, preparing the secretory granule to merge with the plasma membrane. The resulting exocytosis creates a route for rapid cargo release at the appropriate cellular site, linking recognition of a target or stimulus to an immediate immune response.
SNARE proteins are core components of the machinery that joins the granule membrane to the plasma membrane. After signaling activates vesicle priming, these proteins help bring the two membranes together closely enough to fuse. Their activity therefore connects calcium-dependent activation with exocytosis, allowing stored immune mediators to leave the cell rather than remain enclosed in the granule.
Cytosolic calcium provides a signal that couples antigen-receptor engagement to the fusion process. Its rise activates the molecular steps required for vesicle priming and membrane joining, helping prevent release before the immune cell receives an appropriate stimulus. This coupling supports rapid but regulated secretion, which is essential when immune cells must respond at targeted sites.
Fusion enables immune cells to concentrate potent stored molecules at specific locations instead of releasing them indiscriminately. Cytotoxic lymphocytes can deliver perforin and granzymes for targeted cell killing, while mast cells can release histamine and other leukocytes can discharge antimicrobial substances. This spatial control helps coordinate pathogen defense and inflammation with the responding cell or site.
Cytotoxic lymphocytes, mast cells, and other leukocytes use this secretory pathway, but their released cargo reflects different immune functions. Cytotoxic lymphocytes discharge perforin and granzymes, mast cells release histamine, and other leukocytes can deliver antimicrobial substances. Comparing these cell types helps relate a shared fusion mechanism to killing, inflammatory signaling, or pathogen control.
Investigating these transient structures can show how signaling, vesicle priming, and membrane fusion coordinate immune secretion. It can also help identify mechanisms that fail in immunodeficiency, where pathogen defense may be impaired, or contribute to inflammatory disease, where mediator release may be poorly controlled. The process therefore provides a mechanistic link between cellular secretion and disease-related immune outcomes.
The process explains how immune cells convert antigen recognition into localized release of molecules that kill targets, restrict pathogens, or promote inflammation. In infection research, this connects intracellular signaling and exocytosis with antimicrobial defense. In immunology, it clarifies how distinct leukocytes use related membrane-fusion machinery to produce different outcomes, including targeted cytotoxicity and inflammatory responses.