Probing the mechanism of fusion in a two-dimensional computer simulation.
A two-dimensional (2D) model of lipid bilayers was developed and used to investigate a possible role of membrane lateral tension in membrane fusion. We found that an increase of lateral tension in contacting monolayers of 2D analogs of liposomes and planar membranes could cause not only hemifusion, but also complete fusion when internal pressure is introduced in the model. With a certain set of model parameters it was possible to induce hemifusion-like structural changes by a tension increase in only one of the two contacting bilayers. The effect of lysolipids was modeled as an insertion of a small number of extra molecules into the cis or trans side of the interacting bilayers at different stages of simulation. It was found that cis insertion arrests fusion and trans insertion has no inhibitory effect on fusion. The possibility of protein participation in tension-driven fusion was tested in simulation, with one of two model liposomes containing a number of structures capable of reducing the area occupied by them in the outer monolayer. It was found that condensation of these structures was sufficient to produce membrane reorganization similar to that observed in simulations with "protein-free" bilayers. These data support the hypothesis that changes in membrane lateral tension may be responsible for fusion in both model phospholipid membranes and in biological protein-mediated fusion.
Chanturiya
Alexandr
A
Genetic Therapy Inc., Gaithersburg, Maryland 20878, USA. chanturia@nih.gov
Scaria
Puthurapamil
P
Kuksenok
Oleksandr
O
Woodle
Martin C
MC
D055592:Biophysical Phenomena; D001703:Biophysics; D003198:Computer Simulation; D008051:Lipid Bilayers / Q000737:chemistry; D008561:Membrane Fusion / Q000502:physiology*; D008565:Membrane Proteins / Q000737:chemistry / Q000502:physiology; D008954:Models, Biological; D011312:Pressure; D013500:Surface Tension
D008051:Lipid Bilayers; D008565:Membrane Proteins