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Membrane tension and peripheral protein density mediate membrane shape transitions.
1Department of Chemistry, University of Pennsylvania, 231 South 34th Street, Philadelphia, Pennsylvania 19104, USA.
Nature Communications
|January 9, 2015
Summary
Membrane tension reduction triggers ultrafast endocytosis (UFE) by initiating membrane budding and tubulation via proteins like endophilin A1. This discovery explains rapid cellular internalization and provides a model for various endocytic proteins.
Area of Science:
- Cell biology
- Biophysics
- Membrane dynamics
Background:
- Endocytosis is a vital eukaryotic process for membrane trafficking and homeostasis.
- The coupling mechanism between exocytosis and endocytosis remains poorly understood.
- Ultrafast endocytosis (UFE) offers a rapid alternative to classical clathrin-mediated endocytosis (CME).
Purpose of the Study:
- To investigate the role of membrane tension reduction in activating rapid endocytosis.
- To elucidate the mechanism by which endocytic proteins mediate membrane budding and tubulation.
- To develop a quantitative model for membrane shape stability during endocytosis.
Main Methods:
- Experimental manipulation of membrane tension.
- Observation of membrane budding and tubulation using advanced microscopy.
- Quantitative modeling of protein-mediated membrane dynamics.
Main Results:
- Membrane tension reduction was experimentally shown to initiate membrane budding and tubulation.
- Endocytic proteins, specifically endophilin A1, were identified as key mediators.
- Shape instabilities were observed at specific membrane tensions and protein densities, leading to a membrane shape stability diagram.
Conclusions:
- Membrane tension reduction is a critical trigger for ultrafast endocytosis.
- A quantitative model accurately describes membrane shape stability driven by curvature-coupling proteins.
- This model has broad applicability to various endocytic proteins and mechanisms.
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