Sandra A, Leon M A, Przybylski R J
J Cell Sci. 1977 Dec;28:251-72. doi: 10.1242/jcs.28.1.251.
Experimental evidence is presented which is consistent with the involvement of membrane fluidity during myoblast fusion. Treatment of pretrypsinized myoblasts with tetrameric Con A, but not with the dimeric succinyl derivate, inhibits fusion. Inhibition is reversed by treatment with alpha-methyl-D-mannoside or subsequent trypsinization. No inhibition is observed when the lectin is incubated with cells at 4 degrees C unless the incubation is followed by treatment with glycogen, a multivalent Con A cross-linking agent. This effect of glycogen is reversed by subsequent treatment with alpha-amylase. Direct observation of Con A-binding site topography by transmission electron microscopy of membrane replicas of cells labelled with Con A and haemocyanin reveals that inhibition of fusion correlates with a clustered distribution of Con A-binding sites, whereas normal fusion correlates with a dispersed distribution.
本文提供的实验证据表明，成肌细胞融合过程中膜流动性与之相关。用四聚体伴刀豆球蛋白A（Con A）而非二聚体琥珀酰衍生物处理胰蛋白酶预处理过的成肌细胞，会抑制融合。用α-甲基-D-甘露糖苷处理或随后进行胰蛋白酶处理可逆转抑制作用。当凝集素在4℃与细胞孵育时，除非随后用糖原（一种多价Con A交联剂）处理，否则未观察到抑制作用。糖原的这种作用可通过随后用α-淀粉酶处理而逆转。通过对用Con A和血蓝蛋白标记的细胞的膜复制品进行透射电子显微镜直接观察Con A结合位点拓扑结构，发现融合抑制与Con A结合位点的聚集分布相关，而正常融合与分散分布相关。
