Department of Physics, University of South Florida, Tampa, Florida 33620, USA.
J Chem Phys. 2013 Sep 28;139(12):121901. doi: 10.1063/1.4811343.
Deposits of fibrils formed by disease-specific proteins are the molecular hallmark of such diverse human disorders as Alzheimer's disease, type II diabetes, or rheumatoid arthritis. Amyloid fibril formation by structurally and functionally unrelated proteins exhibits many generic characteristics, most prominently the cross β-sheet structure of their mature fibrils. At the same time, amyloid formation tends to proceed along one of two separate assembly pathways yielding either stiff monomeric filaments or globular oligomers and curvilinear protofibrils. Given the focus on oligomers as major toxic species, the very existence of an oligomer-free assembly pathway is significant. Little is known, though, about the structure of the various intermediates emerging along different pathways and whether the pathways converge towards a common or distinct fibril structures. Using infrared spectroscopy we probed the structural evolution of intermediates and late-stage fibrils formed during in vitro lysozyme amyloid assembly along an oligomeric and oligomer-free pathway. Infrared spectroscopy confirmed that both pathways produced amyloid-specific β-sheet peaks, but at pathway-specific wavenumbers. We further found that the amyloid-specific dye thioflavin T responded to all intermediates along either pathway. The relative amplitudes of thioflavin T fluorescence responses displayed pathway-specific differences and could be utilized for monitoring the structural evolution of intermediates. Pathway-specific structural features obtained from infrared spectroscopy and Thioflavin T responses were identical for fibrils grown at highly acidic or at physiological pH values and showed no discernible effects of protein hydrolysis. Our results suggest that late-stage fibrils formed along either pathway are amyloidogenic in nature, but have distinguishable structural fingerprints. These pathway-specific fingerprints emerge during the earliest aggregation events and persist throughout the entire cascade of aggregation intermediates formed along each pathway.
由疾病特异性蛋白形成的纤维沉积物是多种人类疾病(如阿尔茨海默病、2 型糖尿病或类风湿性关节炎)的分子特征。结构和功能上不相关的蛋白质的淀粉样纤维形成表现出许多通用特征,最突出的是其成熟纤维的交叉 β-片层结构。同时,淀粉样形成倾向于沿着两种独立的组装途径之一进行,产生刚性的单体纤维或球状寡聚物和曲线原纤维。鉴于寡聚物作为主要毒性物质的焦点,组装途径中不存在寡聚物的情况是非常重要的。然而,对于沿着不同途径出现的各种中间体的结构以及途径是否收敛到共同或不同的纤维结构,我们知之甚少。使用红外光谱,我们探测了溶菌酶淀粉样体组装过程中在寡聚体和无寡聚体途径中形成的中间体和晚期纤维的结构演变。红外光谱证实,这两种途径都产生了淀粉样体特异性的β-片层峰,但在途径特异性的波数上。我们进一步发现,淀粉样体特异性染料硫代黄素 T 对任何一种途径的所有中间体都有反应。硫代黄素 T 荧光响应的相对幅度显示出途径特异性差异,可用于监测中间体的结构演变。从红外光谱和硫代黄素 T 响应获得的途径特异性结构特征在高酸性或生理 pH 值下生长的纤维中是相同的,并且没有显示出蛋白质水解的可察觉影响。我们的结果表明,沿着任何一种途径形成的晚期纤维本质上是淀粉样的,但具有可区分的结构指纹。这些途径特异性的指纹出现在最早的聚集事件中,并在沿着每条途径形成的整个聚集中间体级联过程中持续存在。