Molecular control of vesicle aggregation and membrane fusion: hypotheses on bile vesicles.
Molecular factors that control the aggregation and fusion of phospholipid vesicles are reviewed. These include membrane composition, vesicle size, various cations, membrane phase state, dehydrating agents and proteins. Several hypotheses are presented for the mechanism by which bile vesicles aggregate and fuse. It is proposed that phase-separated domains of cholesterol in the bile vesicle bilayer mediate the close approach of the vesicles and that molecular packing defects at the domain boundaries mediate hydrophobic interaction between and fusion of apposed membranes. The apposition or fusion of the membranes may provide the third dimension within which the cholesterol domains on apposed or collapsed membranes can begin to form the monohydrate crystal. Other mediators of aggregation and fusion are likely to be proteins that interact hydrophobically with the bile vesicle and diacylglycerol formed in the vesicles by phospholipase C action. Ca2+ is thought to enhance fusion by interacting with bile salts in the membrane or with membrane-associated proteins.
Düzgüneş
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Cancer Research Institute, University of California, San Francisco 94143-0128.
D000818:Animals; D000838:Anions / Q000494:pharmacology; D001646:Bile / Q000378:metabolism*; D002135:Calcium-Binding Proteins / Q000494:pharmacology; D002412:Cations / Q000378:metabolism / Q000494:pharmacology; D006801:Humans; D037102:Lectins / Q000494:pharmacology; D050356:Lipid Metabolism; D008081:Liposomes / Q000378:metabolism; D008561:Membrane Fusion / Q000502:physiology*; D008566:Membranes / Q000378:metabolism; D008954:Models, Biological
D000838:Anions; D002135:Calcium-Binding Proteins; D002412:Cations; D037102:Lectins; D008081:Liposomes