Traub P, Vorgias C E
J Cell Sci. 1983 Sep;63:43-67. doi: 10.1242/jcs.63.1.43.
The potential to form intermediate filaments of a 54 X 10(3) molecular weight (Mr) polypeptide derived from vimentin by cleavage by the intermediate filament-specific, Ca2+-activated proteinase was investigated. Under physiological conditions of assembly, the breakdown product did not form intermediate filaments. Electron microscopy revealed short, rod-like structures similar to those described by Geisler et al. for a 38 X 10(3) Mr alpha-helical core particle derived from desmin. Since the specific, Ca2+-activated proteinase degrades vimentin preferentially from its N terminus, this result suggests the involvement of the basic, N-terminal polypeptide of vimentin in the assembly of intermediate filaments. This was supported by the observation that arginine inhibits the formation of intermediate filaments from intact vimentin. Whereas lysine had very little effect on the assembly process, guanidinium hydrochloride was effective at the same concentration as arginine. On the basis of these findings, an affinity chromatography method for the identification and isolation of intermediate filament subunit proteins was developed. Beside vimentin, desmin, the 68 X 10(3) Mr neurofilament triplet protein, the glial fibrillary acidic protein and cytokeratins also bound to arginine methylester Sepharose 4B in a salt-stable manner and could be eluted with arginine. The 145 X 10(3) Mr neurofilament triplet protein exhibited reduced binding activity, whereas the 210 X 10(3) Mr subunit did not bind to the affinity matrix. Among the degradation products of vimentin produced by the specific, Ca2+-activated proteinase, only those with molecular weights higher than 40 X 10(3) bound to arginine methylester Sepharose 4B. The same applied to the high molecular weight degradation products of desmin with a protein-resistant 37 X 10(3) Mr polypeptide as the major component. The results suggest that arginine residues of the non-alpha-helical, N-terminal polypeptides of intermediate filament subunit proteins play an important role in filament assembly.
研究了由波形蛋白经中间丝特异性、Ca2+激活蛋白酶切割产生的分子量为54×10(3)(Mr)的多肽形成中间丝的潜力。在生理组装条件下,降解产物未形成中间丝。电子显微镜显示出短的棒状结构,类似于Geisler等人描述的源自结蛋白的38×10(3) Mrα-螺旋核心颗粒。由于特异性的Ca2+激活蛋白酶优先从波形蛋白的N端降解,该结果表明波形蛋白的碱性N端多肽参与中间丝的组装。这一观点得到以下观察结果的支持:精氨酸抑制完整波形蛋白形成中间丝。赖氨酸对组装过程影响很小,而盐酸胍在与精氨酸相同浓度时有效。基于这些发现,开发了一种用于鉴定和分离中间丝亚基蛋白的亲和层析方法。除波形蛋白外,结蛋白、68×10(3) Mr神经丝三联体蛋白、胶质纤维酸性蛋白和细胞角蛋白也以盐稳定的方式与精氨酸甲酯琼脂糖4B结合,并可用精氨酸洗脱。145×10(3) Mr神经丝三联体蛋白的结合活性降低,而210×10(3) Mr亚基不与亲和基质结合。在特异性Ca2+激活蛋白酶产生的波形蛋白降解产物中,只有分子量高于40×10(3)的产物与精氨酸甲酯琼脂糖4B结合。这同样适用于以抗蛋白酶的37×10(3) Mr多肽为主要成分的结蛋白高分子量降解产物。结果表明,中间丝亚基蛋白非α-螺旋N端多肽的精氨酸残基在丝组装中起重要作用。