| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
Biophys J, May 2000, p. 2241-2256, Vol. 78, No. 5
and
*Frumkin Institute of Electrochemistry, Moscow, Russia;
Laboratory of Cellular and Molecular Biophysics, National
Institutes of Child Health and Human Development, Bethesda, Maryland
20892 USA; and Department of Molecular Biophysics and
Physiology, Rush Medical College, Chicago, Illinois 60612 USA
The energetics underlying the expansion of fusion pores
connecting biological or lipid bilayer membranes is elucidated. The energetics necessary to deform membranes as the pore enlarges, in some
combination with the action of the fusion proteins, must determine pore
growth. The dynamics of pore growth is considered for the case of two
homogeneous fusing membranes under different tensions. It is rigorously
shown that pore growth can be quantitatively described by treating the
pore as a quasiparticle that moves in a medium with a viscosity
determined by that of the membranes. Motion is subject to tension,
bending, and viscous forces. Pore dynamics and lipid flow through the
pore were calculated using Lagrange's equations, with dissipation
caused by intra- and intermonolayer friction. These calculations show
that the energy barrier that restrains pore enlargement depends only on
the sum of the tensions; a difference in tension between the fusing
membranes is irrelevant. In contrast, lipid flux through the fusion
pore depends on the tension difference but is independent of the sum.
Thus pore growth is not affected by tension-driven lipid flux from one
membrane to the other. The calculations of the present study explain
how increases in tension through osmotic swelling of vesicles cause enlargement of pores between the vesicles and planar bilayer membranes. In a similar fashion, swelling of secretory granules after fusion in
biological systems could promote pore enlargement during exocytosis. The calculations also show that pore expansion can be caused by pore
lengthening; lengthening may be facilitated by fusion proteins.
Biophys J, May 2000, p. 2241-2256, Vol. 78, No. 5
© 2000 by the Biophysical Society 0006-3495/00/05/2241/16 $2.00
This article has been cited by other articles:
 |
|
 |
|
  C. Amatore, S. Arbault, I. Bonifas, Y. Bouret, M. Erard, A. G. Ewing, and L. A. Sombers Correlation between Vesicle Quantal Size and Fusion Pore Release in Chromaffin Cell Exocytosis Biophys. J., June 1, 2005; 88(6): 4411 - 4420. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 V. P. Nikolski and I. R. Efimov Electroporation of the heart Europace, January 1, 2005; 7(s2): S146 - S154. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. A. Sombers, H. J. Hanchar, T. L. Colliver, N. Wittenberg, A. Cans, S. Arbault, C. Amatore, and A. G. Ewing The Effects of Vesicular Volume on Secretion through the Fusion Pore in Exocytotic Release from PC12 Cells J. Neurosci., January 14, 2004; 24(2): 303 - 309. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. Hed and S. A. Safran Initiation and Dynamics of Hemifusion in Lipid Bilayers Biophys. J., July 1, 2003; 85(1): 381 - 389. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. V. Samsonov, P. K. Chatterjee, V. I. Razinkov, C. H. Eng, M. Kielian, and F. S. Cohen Effects of Membrane Potential and Sphingolipid Structures on Fusion of Semliki Forest Virus J. Virol., November 13, 2002; 76(24): 12691 - 12702. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. P. Troyer and R. M. Wightman Temporal Separation of Vesicle Release from Vesicle Fusion during Exocytosis J. Biol. Chem., August 2, 2002; 277(32): 29101 - 29107. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
