Golsteyn R M, Waisman D M
Department of Medical Biochemistry, University of Calgary, Alberta, Canada.
Biochem J. 1989 Feb 1;257(3):817-22. doi: 10.1042/bj2570817.
In the preceding paper [Golsteyn & Waisman (1989) Biochem. J. 257, 809-815] an EGTA-stable, Ca2+-binding heterodimer comprised of a 50 kDa protein and actin called '50K-A' was identified in the unfertilized eggs of the sea urchin Strongylocentrotus purpuratus. In the present paper we have documented the binding of 50K-A to DNAase I and the effect of 50K-A on the kinetics of actin polymerization. When 50K-A was added to pyrene-labelled rabbit skeletal-muscle actin and the salt concentration increased, the initial rate of actin polymerization was inhibited by a very low molar ratio of 50K-A to actin. Furthermore, the steady-state level of G-actin was increased in the presence of 50K-A, suggesting that 50K-A caps the preferred end of actin polymer, shifting the steady-state concentration to that of the non-preferred end. Dilution of F-actin to below its critical concentration into 50K-A resulted in a much slower rate of depolymerization, consistent with capping of the preferred end. In contrast with the Ca2+-dependent binding to DNAase, the effect of 50K-A on the kinetics of actin assembly and disassembly was Ca2+-independent. These results suggest that 50K-A is a novel actin-binding protein with some similarities to the severin/fragmin/gelsolin family of F-actin-capping proteins.
在前一篇论文中[戈尔斯坦 & 魏斯曼(1989年)《生物化学杂志》257卷,809 - 815页],在紫球海胆未受精卵中鉴定出一种由50 kDa蛋白质和肌动蛋白组成的EGTA稳定型Ca²⁺结合异二聚体,称为“50K - A”。在本文中,我们记录了50K - A与脱氧核糖核酸酶I的结合以及50K - A对肌动蛋白聚合动力学的影响。当将50K - A添加到芘标记的兔骨骼肌肌动蛋白中且盐浓度增加时,极低摩尔比的50K - A与肌动蛋白就能抑制肌动蛋白聚合的初始速率。此外,在存在50K - A的情况下,G - 肌动蛋白的稳态水平升高,这表明50K - A封闭了肌动蛋白聚合物的优势末端,将稳态浓度转移到非优势末端。将F - 肌动蛋白稀释至其临界浓度以下并加入50K - A后,解聚速率要慢得多,这与优势末端的封闭情况一致。与依赖Ca²⁺与脱氧核糖核酸酶结合不同,50K - A对肌动蛋白组装和解聚动力学的影响不依赖Ca²⁺。这些结果表明,50K - A是一种新型肌动蛋白结合蛋白,与F - 肌动蛋白封闭蛋白的肌动蛋白切割蛋白/凝溶胶蛋白家族有一些相似之处。