Department of Biochemistry and Biophysics & Program in Molecular and Cellular Biophysics, University of North Carolina at Chapel Hill, North Carolina 27599-7260.
Biophys J. 2013 Dec 3;105(11):2495-506. doi: 10.1016/j.bpj.2013.10.010.
Viral fusion peptides are short N-terminal regions of type-1 viral fusion proteins that are critical for virus entry. Although the importance of viral fusion peptides in virus-cell membrane fusion is established, little is known about how they function. We report the effects of wild-type (WT) hemagglutinin (HA) fusion peptide and its G1S, G1V, and W14A mutants on the kinetics of poly(ethylene glycol)(PEG)-mediated fusion of small unilamellar vesicles composed of dioleoylphosphatidylcholine, dioleoylphosphatidylethanolamine, sphingomyelin, and cholesterol (molar ratio of 35:30:15:20). Time courses of lipid mixing, content mixing, and content leakage were obtained using fluorescence assays at multiple temperatures and analyzed globally using either a two-step or three-step sequential ensemble model of the fusion process to obtain the rate constant and activation thermodynamics of each step. We also monitored the influence of peptides on bilayer interfacial order, acyl chain order, bilayer free volume, and water penetration. All these data were considered in terms of a recently published mechanistic model for the thermodynamic transition states for each step of the fusion process. We propose that WT peptide catalyzes Step 1 by occupying bilayer regions vacated by acyl chains that protrude into interbilayer space to form the Step 1 transition state. It also uniquely contributes a positive intrinsic curvature to hemi-fused leaflets to eliminate Step 2 and catalyzes Step 3 by destabilizing the highly stressed edges of the hemi-fused microstructures that dominate the ensemble of the intermediate state directly preceding fusion pore formation. Similar arguments explain the catalytic and inhibitory properties of the mutant peptides and support the hypothesis that the membrane-contacting fusion peptide of HA fusion protein is key to its catalytic activity.
病毒融合肽是 I 型病毒融合蛋白的短 N 端区域,对病毒进入至关重要。尽管病毒融合肽在病毒-细胞膜融合中的重要性已得到确立,但人们对其功能知之甚少。我们报告了野生型(WT)血凝素(HA)融合肽及其 G1S、G1V 和 W14A 突变体对聚乙二醇(PEG)介导的由二油酰基磷脂酰胆碱、二油酰基磷脂酰乙醇胺、神经鞘磷脂和胆固醇组成的小单层囊泡融合的动力学的影响(摩尔比为 35:30:15:20)。使用荧光测定法在多个温度下获得了脂质混合、内容物混合和内容物泄漏的时间过程,并使用融合过程的两步或三步连续集合模型全局分析,以获得每个步骤的速率常数和活化热力学。我们还监测了肽对双层界面有序性、酰基链有序性、双层自由体积和水渗透的影响。所有这些数据都考虑了最近发表的融合过程每一步热力学过渡态的机制模型。我们提出 WT 肽通过占据由突入双层间空间的酰基链腾空的双层区域来催化步骤 1,从而形成步骤 1 过渡态。它还独特地为半融合的小叶贡献正的固有曲率,以消除步骤 2,并通过使主导融合孔形成之前的中间状态集合的半融合微结构的高度紧张边缘失稳来催化步骤 3。类似的论点解释了突变肽的催化和抑制特性,并支持 HA 融合蛋白的膜接触融合肽是其催化活性关键的假设。