Auclair Jared R, Green Karin M, Shandilya Shivender, Evans James E, Somasundaran Mohan, Schiffer Celia A
Department of Biochemistry and Molecular Pharmacology, University of Massachusetts Medical School, Worcester, Massachusetts 01655, USA.
Proteins. 2007 Nov 1;69(2):270-84. doi: 10.1002/prot.21471.
HIV-1 Vif, an accessory protein in the viral genome, performs an important role in viral pathogenesis by facilitating the degradation of APOBEC3G, an endogenous cellular inhibitor of HIV-1 replication. In this study, intrinsically disordered regions are predicted in HIV-1 Vif using sequence-based algorithms. Intrinsic disorder may explain why traditional structure determination of HIV-1 Vif has been elusive, making structure-based drug design impossible. To characterize HIV-1 Vif's structural topology and to map the domains involved in oligomerization we used chemical cross-linking, proteolysis, and mass spectrometry. Cross-linking showed evidence of monomer, dimer, and trimer species via denaturing gel analysis and an additional tetramer via western blot analysis. We identified 47 unique linear peptides and 24 (13 intramolecular; 11 intermolecular) noncontiguous, cross-linked peptides, among the noncross-linked monomer, cross-linked monomer, cross-linked dimer, and cross-linked trimer samples. Almost complete peptide coverage of the N-terminus is observed in all samples analyzed, however reduced peptide coverage in the C-terminal region is observed in the dimer and trimer samples. These differences in peptide coverage or "protections" between dimer and trimer indicate specific differences in packing between the two oligomeric forms. Intramolecular cross-links within the monomer suggest that the N-terminus is likely folded into a compact domain, while the C-terminus remains intrinsically disordered. Upon oligomerization, as evidenced by the intermolecular cross-links, the C-terminus of one Vif protein becomes ordered by wrapping back on the N-terminal domain of another. In addition, the majority of the intramolecular cross-links map to regions that have been previously reported to be necessary for viral infectivity. Thus, this data suggests HIV-1 Vif is in a dynamic equilibrium between the various oligomers potentially allowing it to interact with other binding partners.
HIV-1 Vif是病毒基因组中的一种辅助蛋白,通过促进APOBEC3G(一种HIV-1复制的内源性细胞抑制剂)的降解,在病毒发病机制中发挥重要作用。在本研究中,使用基于序列的算法预测HIV-1 Vif中的内在无序区域。内在无序可能解释了为什么HIV-1 Vif的传统结构测定一直难以捉摸,使得基于结构的药物设计无法实现。为了表征HIV-1 Vif的结构拓扑并绘制参与寡聚化的结构域,我们使用了化学交联、蛋白水解和质谱分析。通过变性凝胶分析,交联显示出单体、二聚体和三聚体物种的证据,通过蛋白质印迹分析还显示出额外的四聚体。在未交联的单体、交联的单体、交联的二聚体和交联的三聚体样品中,我们鉴定出47个独特的线性肽和24个(13个分子内;11个分子间)不连续的交联肽。在所有分析的样品中都观察到N端几乎完全的肽覆盖,然而在二聚体和三聚体样品中观察到C端区域的肽覆盖减少。二聚体和三聚体之间肽覆盖或“保护”的这些差异表明两种寡聚形式之间堆积的特定差异。单体中的分子内交联表明N端可能折叠成一个紧凑的结构域,而C端仍然是内在无序的。寡聚化时,如分子间交联所证明的,一个Vif蛋白的C端通过回绕到另一个的N端结构域上而变得有序。此外,大多数分子内交联映射到先前报道的对病毒感染性必需的区域。因此,这些数据表明HIV-1 Vif在各种寡聚体之间处于动态平衡,这可能使其能够与其他结合伙伴相互作用。