Itzhaki L S, Neira J L, Ruiz-Sanz J, de Prat Gay G, Fersht A R
MRC Unit for Protein Function and Design Cambridge Centre for Protein Engineering, University Chemical Laboratory, UK.
J Mol Biol. 1995 Nov 24;254(2):289-304. doi: 10.1006/jmbi.1995.0617.
There is a region of well-ordered structure in the transition state of folding of chymotrypsin inhibitor 2 (CI2) that consists of N-terminal residues in the unique alpha-helix (residues 12 to 24) plus some long range interactions, in particular those of Ala16 with Ile57 and Leu49 in the hydrophobic core. This is proposed to be a nucleation site. A crucial question for understanding the initiation of protein folding is: when is the nucleation site formed? Is the alpha-helix pre-formed in the nominally unfolded state, or does it require long-range interactions to be stabilized? To answer this question, we have characterized a series of N-terminal fragments of CI2, each containing an increasing number of subsets of the regular secondary structure. Four small fragments have been examined by circular dichroism and two-dimensional 1H and 15N NMR spectroscopy. The smallest, [1-5], comprises the sequence corresponding to the first beta-strand of the intact protein; the second, [1-13], contains also a type III reverse turn, the second beta-strand, and a type II reverse turn; the third [1-25], consists additionally of the sequence corresponding to the alpha-helix (residues 12 to 24); the fourth, [1-28], contains, in addition, the turn following the alpha-helix. All the fragments have disordered, non-compact structure in aqueous solution. In the structure-promoting co-solvent, trifluoroethanol, alpha-helical structure is stabilized in [1-25] and [1-28] in the region corresponding to the alpha-helix in the intact protein; however, the helix is frayed at both ends and is only fractionally populated, being in dynamic equilibrium with extended conformations. These observations indicate that there is little drive for independent formation of local secondary structure in CI2, and this is reflected in the highly concerted nature of the folding reaction of this protein. The nucleation site of folding of CI2 does not accumulate in the starting state for the folding reaction, but remains embryonic until there are sufficient long range interactions to stabilize it.
在胰凝乳蛋白酶抑制剂2(CI2)折叠的过渡态中,存在一个结构有序的区域,它由独特α-螺旋中的N端残基(残基12至24)以及一些长程相互作用组成,特别是Ala16与疏水核心中的Ile57和Leu49之间的相互作用。这被认为是一个成核位点。理解蛋白质折叠起始的一个关键问题是:成核位点何时形成?α-螺旋是在名义上的未折叠状态下预先形成的,还是需要长程相互作用来稳定?为了回答这个问题,我们对一系列CI2的N端片段进行了表征,每个片段包含越来越多的规则二级结构子集。通过圆二色性以及二维1H和15N核磁共振光谱对四个小片段进行了研究。最小的片段[1-5]包含与完整蛋白质的第一条β链相对应的序列;第二个片段[1-13]还包含一个III型反向转角、第二条β链和一个II型反向转角;第三个片段[1-25]还额外包含与α-螺旋(残基12至24)相对应的序列;第四个片段[1-28]除此之外还包含α-螺旋之后的转角。所有片段在水溶液中都具有无序、非紧密的结构。在促进结构形成的共溶剂三氟乙醇中,与完整蛋白质中的α-螺旋相对应的区域,α-螺旋结构在[1-25]和[1-28]中得到稳定;然而,螺旋两端都有松散,且仅部分占据,与伸展构象处于动态平衡。这些观察结果表明,CI2中局部二级结构的独立形成几乎没有驱动力,这反映在该蛋白质折叠反应的高度协同性质上。CI2折叠的成核位点在折叠反应的起始状态中不会积累,而是保持雏形,直到有足够的长程相互作用来稳定它。