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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...
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A Model Membrane Platform for Reconstituting Mitochondrial Membrane Dynamics
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Value of models for membrane budding.

Christopher T Lee1, Matthew Akamatsu2, Padmini Rangamani1

  • 1Department of Mechanical and Aerospace Engineering, University of California San Diego Jacobs School of Engineering, 9500 Gilman Drive #0411, La Jolla, CA, 92093, USA.

Current Opinion in Cell Biology
|March 11, 2021
PubMed
Summary
This summary is machine-generated.

Computational models illuminate the molecular mechanisms and protein dynamics driving membrane budding during clathrin-mediated endocytosis, enhancing our understanding of cellular trafficking.

Keywords:
Bending modulusBuddingClathrin-mediated endocytosisHelfrichMembrane tensionMultiscale modelingSnapthrough instability

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Area of Science:

  • Cell biology
  • Biophysics
  • Computational biology

Background:

  • Membrane budding and curvature generation are fundamental to cellular trafficking.
  • Clathrin-mediated endocytosis is a well-studied model system for membrane trafficking.
  • Recent advances in experimental techniques offer new insights into protein machinery and membrane dynamics.

Purpose of the Study:

  • To discuss the contributions of computational models to understanding endocytosis.
  • To identify opportunities for integrating models with experimental data.
  • To explore the mechanical principles underlying clathrin-mediated endocytosis.

Main Methods:

  • Review of computational modeling approaches in endocytosis research.
  • Analysis of experimental data on protein machinery and membrane curvature.
  • Discussion of targeted experimental perturbations of cellular membranes.

Main Results:

  • Computational models provide mechanistic insights into clathrin-mediated endocytosis.
  • Models aid in interpreting experimental measurements, especially for membrane perturbations.
  • Advances in experimental methods have improved understanding of protein dynamics.

Conclusions:

  • Computational modeling is crucial for mechanistic interpretation in endocytosis.
  • Strengthening the synergy between models and experiments is key for future discoveries.
  • Further integration can advance our knowledge of membrane trafficking and curvature generation.