Endocytosis Switch Controlled by Transmembrane Osmotic Pressure and Phospholipid Number Asymmetry

The dynamics of endocytosis in living K562 cells was investigated after the osmotic pressure of the external medium was decreased and the transmembrane phospholipid number asymmetry was increased. When the external pressure was decreased by a factor of 0.54, a sudden inhibition of endocytosis was ob...

Full description

Saved in:
Bibliographic Details
Published in:Biophysical journal 2000-06, Vol.78 (6), p.3036-3047
Main Authors: Rauch, Cyril, Farge, Emmanuel
Format: Article
Language:English
Subjects:
Cell Behavior
Cell Membrane - physiology
Cells
Cellular Biology
Endocytosis
Humans
K562 Cells
Life Sciences
Lipids
Membrane Lipids - physiology
Membrane Proteins - physiology
Membranes
Models, Biological
Osmosis
Osmotic Pressure
Phospholipids - physiology
Proteins
Subcellular Processes
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:The dynamics of endocytosis in living K562 cells was investigated after the osmotic pressure of the external medium was decreased and the transmembrane phospholipid number asymmetry was increased. When the external pressure was decreased by a factor of 0.54, a sudden inhibition of endocytosis was observed. Under these conditions, the endocytosis suddenly recovered after the phospholipid number asymmetry was increased. The phospholipid asymmetry was generated by the addition of exogenous phosphatidylserine, which is translocated by the endogenous flippase activity to the inner layer of the membrane. The recovery of endocytosis is thus consistent with the view that the phospholipid number asymmetry can act as a budding force for endocytosis. Moreover, we quantitatively predict both the inhibition and recovery of endocytosis as first-order phase transitions, using a general model that assumes the existence of a transmembrane surface tension asymmetry as the budding driving force. In this model, the tension asymmetry is considered to be elastically generated by the activity of phospholipid pumping. We finally propose that cells may trigger genetic transcription responses after the internalization of cytokine-receptor complexes, which could be controlled by variations in the cytosolic or external pressure.
ISSN:0006-3495
1542-0086
DOI:10.1016/S0006-3495(00)76842-1