The interaction of Sendai virus glycoproteins with cell membranes was proposed to increase the lateral mobility of membrane proteins, enabling membrane fusion and the aggregation of intramembrane particles by thermotropic separation (Volsky, D J & Loyter, A, Biochim biophys acta 514 (1978) 213 ; Maeda, T et al. Exp cell res 123 (1979) 333 ; and Kim, J & Okada, Y, Exp cell res 132 (1981) 125 ). In order to test this hypothesis, we employed fluorescence photobleaching recovery to investigate the effects of Sendai virus-induced fusion on the lateral mobility of membrane proteins and lipids in a variety of cell types (human erythrocytes, BHK21, HeLa, 3T3 NIH, and mouse spleen lymphocytes). The results of the lateral diffusion measurements demonstrate that no significant alterations occur in the lateral motion of membrane proteins or a fluorescent phospholipid on all the cell types examined, including cells which revealed high susceptibility to the virally mediated fusion (human erythrocytes and BHK21 cells). These findings suggest that a permanent increase in the lateral mobility of cell surface components does not generally occur during Sendai virus-induced cell fusion, and thus cannot play a role in the fusion mechanism. The possible involvement of transient alterations in the lateral mobility of membrane components in the fusion mechanism is discussed.
Funding Information:This research was supported in part by a grant from the Fund for Basic Research (administered by the Israel Academy of Sciences and Humanities), and by a fellowship (to Y. I. H.) from the Bat-Sheva de Rothschild Fund for the Advancement of Science and Technology.