Fusogenic mechanisms

Abstract

Recent work is described on the fusion of human erythrocytes induced by chlorpromazine, which is accompanied by the endogenous proteolysis of integral and skeletal membrane proteins. This fusion reaction is of interest because it occurs at a high incidence in the presence of EGTA. It thus contrasts with the emphasis that has been placed on the role of Ca2+ in the fusion of lipid bilayers as a model for its behaviour in biomembrane fusion reactions. A survey of fusion in cells induced by chemicals and by Sendai virus, and of fusion in liposomes, in fact reveals numerous reported instances of fusion occurring in the absence of Ca2+. The finding that endogenous proteolysis of erythrocyte membrane proteins accompanies cell fusion induced by chlorpromazine leads to the suggestion that the products of proteolysis may in some cases be fusogenic, and that their formation may provide a general mechanism for the fusion of lipid bilayers in biomembrane fusion reactions, aspects of which are imitated by the fusogenic viruses.