Aroeti B, Henis Y I
Exp Cell Res. 1986 Jan;162(1):243-54. doi: 10.1016/0014-4827(86)90442-8.
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, DJ & Loyter, A, Biochim biophys acta 514 (1978) 213 [13]; Maeda, T et al. Exp cell res 123 (1979) 333 [15]; and Kim, J & Okada, Y, Exp cell res 132 (1981) 125 [44]). 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.
有人提出，仙台病毒糖蛋白与细胞膜的相互作用会增加膜蛋白的侧向流动性，通过热致分离实现膜融合和膜内颗粒聚集（沃尔斯基，DJ和洛伊特，A，《生物化学与生物物理学报》514（1978）213 [13]；前田，T等人，《细胞实验研究》123（1979）333 [15]；以及金，J和冈田，Y，《细胞实验研究》132（1981）125 [44]）。为了验证这一假设，我们采用荧光漂白恢复技术来研究仙台病毒诱导的融合对多种细胞类型（人红细胞、BHK21、HeLa、3T3 NIH和小鼠脾淋巴细胞）中膜蛋白和脂质侧向流动性的影响。侧向扩散测量结果表明，在所检测的所有细胞类型中，包括对病毒介导的融合高度敏感的细胞（人红细胞和BHK21细胞），膜蛋白或荧光磷脂的侧向运动均未发生显著改变。这些发现表明，在仙台病毒诱导的细胞融合过程中，细胞表面成分的侧向流动性通常不会永久性增加，因此在融合机制中不起作用。本文讨论了膜成分侧向流动性的瞬时改变在融合机制中可能的参与情况。
