Hatzfeld M, Weber K
Max Planck Institute for Biophysical Chemistry, Department of Biochemistry, Goettingen, Germany.
J Cell Biol. 1992 Jan;116(1):157-66. doi: 10.1083/jcb.116.1.157.
All intermediate filament (IF) proteins share a highly conserved sequence motif at the COOH-terminal end of their rod domains. We have studied the influence of a 20-residue peptide, representing the consensus motif on filament formation and stability. Addition of the peptide at a 10-20-fold molar excess over keratins K8 plus K18 had a severe effect on subsequent IF assembly. Filaments displayed a rough surface and variable diameters with a substantial amount present in unravelled form. At higher peptide concentration (50-100-fold molar excess), IF formation was completely inhibited and instead only loose aggregates of "globular" particles were formed. The peptide also influenced performed keratin IF in a dose-dependent manner. While a three-fold molar excess was sufficient to cause partial fragmentation of IF, a 50-fold molar excess caused complete disassembly within 5 min. Loosely associated protofibrils, short needlelike IF fragments, and aggregates of globular particles were detected. The motif peptide also caused the disassembly of filaments formed by desmin, a type III IF protein. Peptide concentrations and incubation times required for complete disassembly were somewhat higher than for the filaments containing K8 plus K18. A 50-fold molar excess was sufficient to cause complete disassembly within 1 h. Peptides unrelated in sequence to the motif did not interfere with filament formation or stability even when present for more than 12 h at a 100-fold molar excess. The results suggest that the motif sequence normally binds to a specific acceptor site for which the motif peptide can successfully compete. Taken together with current models of IF structure the results indicate that normal binding of the motif sequence to its acceptor must play an essential role in IF formation, possibly by directing the proper alignment of neighboring tetramers or protofilaments. Finally we show that in vitro formed IF are much more sensitive and dynamic strutures than previously thought.
所有中间丝(IF)蛋白在其杆状结构域的COOH末端共享一个高度保守的序列基序。我们研究了一个代表该共有基序的20个残基的肽对丝形成和稳定性的影响。以比角蛋白K8加K18高10 - 20倍的摩尔过量添加该肽,对随后的IF组装有严重影响。细丝表面粗糙,直径可变,大量以解聚形式存在。在更高的肽浓度(50 - 100倍摩尔过量)下,IF形成被完全抑制,取而代之的是仅形成“球状”颗粒的松散聚集体。该肽还以剂量依赖的方式影响已形成的角蛋白IF。虽然三倍摩尔过量足以导致IF部分断裂,但50倍摩尔过量会在5分钟内导致完全解体。检测到松散相关的原纤维、短针状IF片段和球状颗粒聚集体。该基序肽还导致由结蛋白(一种III型IF蛋白)形成的细丝解体。完全解体所需的肽浓度和孵育时间略高于含K8加K18的细丝。50倍摩尔过量足以在1小时内导致完全解体。与该基序序列无关的肽即使以100倍摩尔过量存在超过12小时也不会干扰细丝形成或稳定性。结果表明,该基序序列通常与一个特定的受体位点结合,基序肽可以成功竞争该位点。结合当前的IF结构模型,结果表明基序序列与其受体的正常结合在IF形成中必须发挥重要作用,可能是通过指导相邻四聚体或原丝的正确排列。最后我们表明,体外形成的IF比以前认为的更敏感且结构更具动态性。