help button home button Biophys. J.
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Rauch, C.
Right arrow Articles by Farge, E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Rauch, C.
Right arrow Articles by Farge, E.

Biophys J, June 2000, p. 3036-3047, Vol. 78, No. 6

Endocytosis Switch Controlled by Transmembrane Osmotic Pressure and Phospholipid Number Asymmetry

Cyril Rauch* and Emmanuel Farge*dagger

 *Groupe "Mécanique et Génétique du Développement Embryonnaire," UMR 168 Physico-Chimie Curie, Institut Curie,  dagger Institut Universitaire de France, 75248 Paris Cedex 05, France

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.

Biophys J, June 2000, p. 3036-3047, Vol. 78, No. 6
© 2000 by the Biophysical Society   0006-3495/00/06/3036/12  $2.00


This article has been cited by other articles:


Home page
 Proc. Natl. Acad. Sci. USAHome page
G. Bao and X. R. Bao
Shedding light on the dynamics of endocytosis and viral budding
PNAS, July 19, 2005; 102(29): 9997 - 9998.
[Full Text] [PDF]

Home page
 J. Cell Sci.Home page
T. Pomorski, J. C. M. Holthuis, A. Herrmann, and G. van Meer
Tracking down lipid flippases and their biological functions
J. Cell Sci., February 22, 2004; 117(6): 805 - 813.
[Abstract] [Full Text] [PDF]

Home page
 Biophys. JHome page
M. Traikia, D. E. Warschawski, O. Lambert, J.-L. Rigaud, and P. F. Devaux
Asymmetrical Membranes and Surface Tension
Biophys. J., September 1, 2002; 83(3): 1443 - 1454.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
X. Zha, J. Genest Jr., and R. McPherson
Endocytosis Is Enhanced in Tangier Fibroblasts. POSSIBLE ROLE OF ATP-BINDING CASSETTE PROTEIN A1 IN ENDOSOMAL VESICULAR TRANSPORT
J. Biol. Chem., October 12, 2001; 276(42): 39476 - 39483.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2000 by the Biophysical Society.