Tranter M P, Sugrue S P, Schwartz M A
Department of Anatomy and Cellular Biology, Harvard Medical School, Boston, Massachusetts.
J Cell Biol. 1989 Dec;109(6 Pt 1):2833-40. doi: 10.1083/jcb.109.6.2833.
We have investigated the association of actin with membranes isolated from rat liver. A plasma membrane-enriched fraction prepared by homogenization in a low salt/CaCl2 buffer was found to contain a substantial amount of residual actin which could be removed by treatment with 1 M Na2CO3/NaHCO3, pH 10.5. Using a sedimentation binding assay that uses gelsolin to shorten actin filaments and render membrane binding saturable (Schwartz, M. A., and E. J. Luna. 1986. J. Cell Biol. 102:2067-2075), we found that membranes stripped of endogenous actin bound 125I-actin in a specific and saturable manner. Scatchard plots of binding data were linear, indicating a single class of binding sites with a Kd of 1.6 microns; 66 micrograms actin bound/mg membrane protein at saturation. Binding of actin to liver cell membranes was negligible with unstripped membranes, was competed by excess unlabeled actin, and was greatly reduced by preheating or proteolytic digestion of the membranes. Kinetic measurements showed that binding had an initial lag phase and was strongly temperature dependent. The binding of actin to liver cell membranes was also found to be competitively inhibited by ATP and other nucleotides, including the nonhydrolyzable analogue AMP-PNP. We conclude that we have reconstituted an interaction between actin and integral membrane proteins from the rat liver. This interaction exhibits a number of distinctive features which have not been observed in other actin-membrane systems.
我们研究了肌动蛋白与从大鼠肝脏分离的膜之间的关联。通过在低盐/CaCl2缓冲液中匀浆制备的富含质膜的部分被发现含有大量残留的肌动蛋白,可用1 M Na2CO3/NaHCO3(pH 10.5)处理将其去除。使用一种沉降结合测定法,该方法利用凝溶胶蛋白缩短肌动蛋白丝并使膜结合达到饱和(施瓦茨,M. A.,和E. J. 卢纳。1986。《细胞生物学杂志》102:2067 - 2075),我们发现去除内源性肌动蛋白的膜以特异性和饱和的方式结合125I - 肌动蛋白。结合数据的斯卡查德图呈线性,表明存在一类结合位点,其解离常数(Kd)为1.6微米;饱和时每毫克膜蛋白结合66微克肌动蛋白。未去除肌动蛋白的膜与肝细胞膜的结合可忽略不计,会被过量未标记的肌动蛋白竞争,并且通过膜的预热或蛋白水解消化会大大降低。动力学测量表明结合有一个初始延迟期且强烈依赖温度。还发现肌动蛋白与肝细胞膜的结合受到ATP和其他核苷酸的竞争性抑制,包括不可水解的类似物AMP - PNP。我们得出结论,我们已经重建了大鼠肝脏中肌动蛋白与整合膜蛋白之间的相互作用。这种相互作用表现出许多在其他肌动蛋白 - 膜系统中未观察到的独特特征。