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单体重组轮状病毒VP4的蛋白水解产生一种寡聚体VP5*核心。

Proteolysis of monomeric recombinant rotavirus VP4 yields an oligomeric VP5* core.

作者信息

Dormitzer P R, Greenberg H B, Harrison S C

机构信息

Laboratory of Molecular Medicine, Children's Hospital, Boston, Massachusetts 02115, USA.

出版信息

J Virol. 2001 Aug;75(16):7339-50. doi: 10.1128/JVI.75.16.7339-7350.2001.

Abstract

Rotavirus particles are activated for cell entry by trypsin cleavage of the outer capsid spike protein, VP4, into a hemagglutinin, VP8*, and a membrane penetration protein, VP5*. We have purified rhesus rotavirus VP4, expressed in baculovirus-infected insect cells. Purified VP4 is a soluble, elongated monomer, as determined by analytical ultracentrifugation. Trypsin cleaves purified VP4 at a number of sites that are protected on the virion and yields a heterogeneous group of protease-resistant cores of VP5*. The most abundant tryptic VP5* core is trimmed past the N terminus associated with activation for virus entry into cells. Sequential digestion of purified VP4 with chymotrypsin and trypsin generates homogeneous VP8* and VP5* cores (VP8CT and VP5CT, respectively), which have the authentic trypsin cleavages in the activation region. VP8CT is a soluble monomer composed primarily of beta-sheets. VP5CT forms sodium dodecyl sulfate-resistant dimers. These results suggest that trypsinization of rotavirus particles triggers a rearrangement in the VP5* region of VP4 to yield the dimeric spikes observed in icosahedral image reconstructions from electron cryomicroscopy of trypsinized rotavirus virions. The solubility of VP5CT and of trypsinized rotavirus particles suggests that the trypsin-triggered conformational change primes VP4 for a subsequent rearrangement that accomplishes membrane penetration. The domains of VP4 defined by protease analysis contain all mapped neutralizing epitopes, sialic acid binding residues, the heptad repeat region, and the membrane permeabilization region. This biochemical analysis of VP4 provides sequence-specific structural information that complements electron cryomicroscopy data and defines targets and strategies for atomic-resolution structural studies.

摘要

轮状病毒颗粒通过胰蛋白酶将外 capsid 刺突蛋白 VP4 切割成血凝素 VP8和膜穿透蛋白 VP5而被激活以进入细胞。我们已经纯化了在杆状病毒感染的昆虫细胞中表达的恒河猴轮状病毒 VP4。通过分析超速离心确定,纯化的 VP4 是一种可溶性的细长单体。胰蛋白酶在病毒体上受保护的多个位点切割纯化的 VP4,并产生一组异质的抗蛋白酶 VP5核心。最丰富的胰蛋白酶 VP5核心在与病毒进入细胞的激活相关的 N 末端之后被修剪。用胰凝乳蛋白酶和胰蛋白酶对纯化的 VP4 进行顺序消化产生均匀的 VP8和 VP5核心(分别为 VP8CT 和 VP5CT),它们在激活区域具有真实的胰蛋白酶切割。VP8CT 是主要由β-折叠组成的可溶性单体。VP5CT 形成抗十二烷基硫酸钠的二聚体。这些结果表明,轮状病毒颗粒的胰蛋白酶处理触发了 VP4 的 VP5*区域的重排,以产生在胰蛋白酶处理的轮状病毒病毒体的电子冷冻显微镜二十面体图像重建中观察到的二聚体刺突。VP5CT 和胰蛋白酶处理的轮状病毒颗粒的溶解性表明,胰蛋白酶触发的构象变化使 VP4 为随后完成膜穿透的重排做好准备。通过蛋白酶分析定义的 VP4 结构域包含所有映射到的中和表位、唾液酸结合残基、七肽重复区域和膜通透区域。对 VP4 的这种生化分析提供了序列特异性结构信息,补充了电子冷冻显微镜数据,并定义了原子分辨率结构研究的目标和策略。

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