Eichinger L, Schleicher M
Max-Planck-Institut für Biochemie, Martinsried, Federal Republic of Germany.
Biochemistry. 1992 May 26;31(20):4779-87. doi: 10.1021/bi00135a006.
Severin is a Ca(2+)-activated actin-binding protein that nucleates actin assembly and severs and caps the fast growing ends of actin filaments. It consists of three highly conserved domains. To investigate the domain structure of severin, we constructed genetically the N-terminal domain 1, the middle domain 2, and the tandem domains 2 + 3. Their interaction with actin, Ca2+, and lipids was characterized. Domain 1 contains the F-actin capping and a Ca(2+)-binding site [Eichinger, L., Noegel, A. A., & Schleicher, M. (1991) J. Cell Biol. 112, 665-676]. Binding of domain 2 to actin filaments was Ca(2+)-dependent and saturated at a 1:1 molar ratio. In the presence of Ca2+, about 1.5 mol of domains 2 + 3 bound per mole of F-actin subunit. Scatchard analysis gave a Kd of 18 microM for the interaction of domain 2 with F-actin subunits and a Kd of 1.6 microM for domains 2 + 3. Low-shear viscometry, electron microscopy, and low-speed sedimentation assays showed that domains 2 + 3 induced bundling of actin filaments. The influence of PIP2 micelles on the different activities of severin was assayed using native severin and N- and C-terminally truncated fragments. Severin contains at least two PIP2-binding sites since the activities of the two nonoverlapping severin fragments domain 1 and domains 2 + 3 were inhibited by PIP2. The specificity of severin-phospholipid interaction was investigated by studying the regulation of native severin by PIP2 and other pure or mixed phospholipids.(ABSTRACT TRUNCATED AT 250 WORDS)
肌割蛋白是一种钙激活的肌动蛋白结合蛋白,它能使肌动蛋白装配成核,并切断和封闭肌动蛋白丝快速生长的末端。它由三个高度保守的结构域组成。为了研究肌割蛋白的结构域结构,我们通过基因手段构建了N端结构域1、中间结构域2以及串联结构域2 + 3。对它们与肌动蛋白、钙离子和脂质的相互作用进行了表征。结构域1包含F - 肌动蛋白封闭位点和一个钙结合位点[艾兴格,L.,内格尔,A. A.,& 施莱歇尔,M.(1991年)《细胞生物学杂志》112卷,665 - 676页]。结构域2与肌动蛋白丝的结合依赖于钙离子,且在1:1摩尔比时达到饱和。在钙离子存在的情况下,每摩尔F - 肌动蛋白亚基约结合1.5摩尔的结构域2 + 3。斯卡查德分析得出结构域2与F - 肌动蛋白亚基相互作用的解离常数为18微摩尔,结构域2 + 3的解离常数为1.6微摩尔。低剪切粘度测定法、电子显微镜和低速沉降分析表明结构域2 + 3能诱导肌动蛋白丝成束。使用天然肌割蛋白以及N端和C端截短片段,测定了磷脂酰肌醇 - 4,5 - 二磷酸(PIP2)微团对肌割蛋白不同活性的影响。肌割蛋白至少包含两个PIP2结合位点,因为两个不重叠的肌割蛋白片段结构域1和结构域2 + 3的活性都受到PIP2的抑制。通过研究PIP2和其他纯的或混合的磷脂对天然肌割蛋白的调节作用,探究了肌割蛋白与磷脂相互作用的特异性。(摘要截选至250词)