Mok Y K, Alonso L G, Lima L M, Bycroft M, de Prat-Gay G
Instituto de Investigaciones Bioquímicas, Fundación Campomar, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Argentina.
Protein Sci. 2000 Apr;9(4):799-811. doi: 10.1110/ps.9.4.799.
The dimeric beta-barrel is a characteristic topology initially found in the transcriptional regulatory domain of the E2 DNA binding domain from papillomaviruses. We have previously described the kinetic folding mechanism of the human HPV-16 domain, and, as part of these studies, we present a structural characterization of the urea-denatured state of the protein. We have obtained a set of chemical shift assignments for the C-terminal domain in urea using heteronuclear NMR methods and found regions with persistent residual structure. Based on chemical shift deviations from random coil values, 3'J(NHN alpha) coupling constants, heteronuclear single quantum coherence peak intensities, and nuclear Overhauser effect data, we have determined clusters of residual structure in regions corresponding to the DNA binding helix and the second beta-strand in the folded conformation. Most of the structures found are of nonnative nature, including turn-like conformations. Urea denaturation at equilibrium displayed a loss in protein concentration dependence, in absolute parallel to a similar deviation observed in the folding rate constant from kinetic experiments. These results strongly suggest an alternative folding pathway in which a dimeric intermediate is formed and the rate-limiting step becomes first order at high protein concentrations. The structural elements found in the denatured state would collide to yield productive interactions, establishing an intermolecular folding nucleus at high protein concentrations. We discuss our results in terms of the folding mechanism of this particular topology in an attempt to contribute to a better understanding of the folding of dimers in general and intertwined dimeric proteins such as transcription factors in particular.
二聚体β-桶是一种独特的拓扑结构,最初在乳头瘤病毒E2 DNA结合结构域的转录调控区域中发现。我们之前描述了人乳头瘤病毒16型结构域的动力学折叠机制,作为这些研究的一部分,我们展示了该蛋白质尿素变性状态的结构特征。我们使用异核核磁共振方法获得了尿素中C末端结构域的一组化学位移归属,并发现了具有持续残余结构的区域。基于与无规卷曲值的化学位移偏差、3J(NHNα)耦合常数、异核单量子相干峰强度和核Overhauser效应数据,我们确定了折叠构象中与DNA结合螺旋和第二条β链相对应区域的残余结构簇。发现的大多数结构是非天然性质的,包括类似转角的构象。平衡时的尿素变性显示出蛋白质浓度依赖性的丧失,这与动力学实验中折叠速率常数观察到的类似偏差完全平行。这些结果强烈表明存在一种替代折叠途径,其中形成二聚体中间体,并且在高蛋白质浓度下限速步骤变为一级反应。在变性状态下发现的结构元件会相互碰撞以产生有效的相互作用,在高蛋白质浓度下建立分子间折叠核心。我们根据这种特定拓扑结构的折叠机制来讨论我们的结果,试图有助于更好地理解一般二聚体的折叠,特别是转录因子等交织二聚体蛋白质的折叠。