Labbé J P, Méjean C, Benyamin Y, Roustan C
UPR 8402, Centre de Recherches de Biochimie Macromoléculaire (CNRS), U249 (INSERM), Université de Montpellier 1, France.
Biochem J. 1990 Oct 15;271(2):407-13. doi: 10.1042/bj2710407.
Evidence for the participation of the 1-7 and 18-28 N-terminal sequences of actin at different steps of actin-myosin interaction process is well documented in the literature. Cross-linking of the rigor complex between filamentous actin and skeletal-muscle myosin subfragment 1 was accomplished by the carboxy-group-directed zero-length protein cross-linker, 1-ethyl-3-[3-(dimethylamino)propyl]carbodi-imide. After chaotropic depolymerization and thrombin digestion, which cleaves only actin, the covalent complex with Mr 100,000 was characterized by PAGE. The linkage was identified as being between myosin subfragment 1 (S-1) heavy chain and actin-(1-28)-peptide. The purified complex retained in toto its ability to combine reversibly with fresh filamentous actin, but showed a decrease in the Vmax. of actin-dependent Mg2(+)-ATPase. By using e.l.i.s.a., S-1 was observed to bind to coated monomeric actin or its 1-226 N-terminal peptide. This interaction strongly interfered with the binding of antibodies directed against the 95-113 actin sequence. Moreover, S-1 was able to bind with coated purified actin-(40-113)-peptide. Finally, antibodies directed against the 18-28 and 95-113 actin sequence, which strongly interfered with S1 binding, were unable to compete with each other. These results suggest that two topologically independent regions are involved in the actin-myosin interface: one located in the conserved 18-28 sequence and the other near residues 95-113, including the variable residue at position 89. Other experiments support the 'multisite interface model', where the two actin sites could modulate each other during S-1 interaction.
肌动蛋白的1-7和18-28 N端序列在肌动蛋白-肌球蛋白相互作用过程的不同步骤中发挥作用的证据在文献中已有充分记载。丝状肌动蛋白与骨骼肌肌球蛋白亚片段1之间的僵直复合物交联是通过羧基导向的零长度蛋白质交联剂1-乙基-3-[3-(二甲氨基)丙基]碳二亚胺完成的。在离液剂解聚和凝血酶消化(仅切割肌动蛋白)后,通过聚丙烯酰胺凝胶电泳(PAGE)对分子量为100,000的共价复合物进行了表征。该连接被确定为在肌球蛋白亚片段1(S-1)重链和肌动蛋白-(1-28)-肽之间。纯化的复合物完全保留了其与新鲜丝状肌动蛋白可逆结合的能力,但肌动蛋白依赖性Mg2(+)-ATP酶的最大反应速度(Vmax)有所降低。通过酶联免疫吸附测定(e.l.i.s.a.),观察到S-1与包被的单体肌动蛋白或其1-226 N端肽结合。这种相互作用强烈干扰了针对肌动蛋白95-至113序列的抗体的结合。此外,S-1能够与包被的纯化肌动蛋白-(40-113)-肽结合。最后,针对18-28和95-113肌动蛋白序列的抗体虽然强烈干扰S1结合,但彼此之间无法相互竞争。这些结果表明,肌动蛋白-肌球蛋白界面涉及两个拓扑独立的区域:一个位于保守的18-28序列中,另一个靠近95-113位残基,包括89位的可变残基。其他实验支持“多位点界面模型”,即在S-1相互作用过程中,两个肌动蛋白位点可能相互调节。