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Related Concept Videos

Pinching-off of Coated Vesicles01:32

Pinching-off of Coated Vesicles

Vesicle budding is orchestrated by distinct cytosolic proteins such as adaptor proteins, coat proteins, and GTPases. To initiate vesicle budding, membrane-bending proteins containing crescent-shaped BAR domains bind to the lipid heads in the bilayer and distort the membrane to form a protein-coated vesicle bud. Adaptors proteins such as AP2 for clathrin-coated vesicles can nucleate on the deformed membrane. Finally, coat proteins such as clathrin or COPI and COPII assemble into a coat forming...
SNAREs and Membrane Fusion01:43

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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...
Asymmetric Lipid Bilayer01:35

Asymmetric Lipid Bilayer

Biological membranes show uneven distribution of different types of lipids in the inner and outer layers, resulting in transverse asymmetric membranes. The treatment of the erythrocyte membrane with the enzyme phospholipase confirmed the asymmetric nature of the lipid bilayer. The enzyme hydrolyzes lipids into fatty acids and hydrophilic groups. The phospholipase acts only on the outer layer of the membrane, while the inner layer remains intact. The phospholipase treatment resulted in 80%...
Vesicular Tubular Clusters01:45

Vesicular Tubular Clusters

After budding out from the ER membrane, some COPII vesicles lose their coat and fuse with one another to form larger vesicles and interconnected tubules called vesicular tubular clusters or VTCs. These clusters constitute a compartment at the ER-Golgi interface known as ERGIC (Endoplasmic Reticulum Golgi Intermediate Compartment). The ERGIC is a mobile membrane-bound cargo transport system that sorts proteins secreted from ER and delivers them to the Golgi.
With the help of motor proteins such...
Mechanism of Lamellipodia Formation01:31

Mechanism of Lamellipodia Formation

Cells migrating in response to external stimuli form lamellipodia, which are thin membrane protrusions supported by a mesh of linked, branched, or unbranched actin filaments. These actin filaments interact with myosin motor proteins, creating the dynamic actomyosin complex within the cytoskeleton. Contractility, or the ability to generate contractile stress, is inherent to the actomyosin complex. It helps cells detect the stiffness of the surrounding ECM and exert contractile force for...
Fusion of Secretory Vesicles with the Plasma Membrane01:26

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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.
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Updated: Jun 19, 2026

Phase Behavior of Charged Vesicles Under Symmetric and Asymmetric Solution Conditions Monitored with Fluorescence Microscopy
10:08

Phase Behavior of Charged Vesicles Under Symmetric and Asymmetric Solution Conditions Monitored with Fluorescence Microscopy

Published on: October 24, 2017

Phase-transition- and dissipation-driven budding in lipid vesicles.

Thomas Franke1, Christian T Leirer, Achim Wixforth

  • 1University of Augsburg, Experimental Physics I, 86159 Augsburg, Germany.

Chemphyschem : a European Journal of Chemical Physics and Physical Chemistry
|October 16, 2009
PubMed
Summary
This summary is machine-generated.

Non-equilibrium membrane budding occurs rapidly under mechanical stress during lipid phase transitions. Dissipation drives multiple bud formation, influenced by membrane and bulk viscosity.

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Published on: January 22, 2019

Area of Science:

  • Biophysics
  • Membrane dynamics
  • Soft matter physics

Background:

  • Membrane budding is typically studied as an equilibrium process.
  • Non-equilibrium budding, especially at short timescales (< tau), is less understood.
  • Lipid phase transitions influence membrane mechanical properties.

Purpose of the Study:

  • To investigate non-equilibrium membrane budding under rapid lipid phase transitions.
  • To explore the role of mechanical perturbations and viscosity in bud formation.
  • To develop a theoretical model for dissipative budding.

Main Methods:

  • Inducing phase transitions in giant unilamellar vesicles (GUVs) via temperature changes.
  • Utilizing short timescales (< tau) to drive non-equilibrium processes.
  • Developing a theoretical model incorporating membrane and bulk viscosity.

Main Results:

  • Localized, rapidly growing non-equilibrium buds form immediately during rapid phase transitions.
  • Buds grow as spherical caps due to hindered in-plane spreading by the gel matrix.
  • Dissipation favors multiple bud formation, with bud size inversely related to bulk viscosity.
  • A critical rate of area change, dependent on viscosity, triggers dissipative budding.

Conclusions:

  • Rapid mechanical perturbations during lipid phase transitions can induce non-equilibrium membrane budding.
  • Viscosity plays a critical role in the number and size of buds formed.
  • The theoretical model accurately predicts the conditions for dissipative budding.