Lin C, Amberg S M, Chambers T J, Rice C M
Department of Molecular Microbiology, Washington University School of Medicine, St. Louis, Missouri 63110-1093.
J Virol. 1993 Apr;67(4):2327-35. doi: 10.1128/JVI.67.4.2327-2335.1993.
Flavivirus proteins are produced by co- and posttranslational proteolytic processing of a large polyprotein by both host- and virus-encoded proteinases. The viral serine proteinase, which consists of NS2B and NS3, is responsible for cleavage of at least four dibasic sites (2A/2B, 2B/3, 3/4A, and 4B/5) in the nonstructural region. Since the amino acid sequence preceding NS4B shares characteristics with signal peptides used for translocation of nascent polypeptides into the lumen of the endoplasmic reticulum, it has been proposed that cleavage at the 4A/4B site is mediated by a cellular signal peptidase. In this report, cell-free translation and in vivo transient expression assays were used to study processing in the NS4 region of the yellow fever virus polyprotein. With a construct which contained NS4B preceded by 17 residues constituting the putative signal peptide (sig4B), membrane-dependent cleavage at the 4A/4B site was demonstrated in vitro. Surprisingly, processing of NS4A-4B was not observed in cell-free translation studies, and in vivo expression of several yellow fever virus polyproteins revealed that the 4A/4B cleavage occurred only during coexpression of NS2B and the proteinase domain of NS3. Examination of mutant derivatives of the NS3 proteinase domain demonstrated that cleavage at the 4A/4B site correlated with expression of an active NS2B-3 proteinase. From these results, we propose a model in which the signalase cleavage generating the N terminus of NS4B requires a prior NS2B-3 proteinase-mediated cleavage at a novel site (called the 4A/2K site) which is conserved among flaviviruses and located 23 residues upstream of the signalase site. In support of this model, mutations at the 4A/4B signalase site did not eliminate processing in the NS4 region. In contrast, substitutions at the 4A/2K site, which were engineered to block NS2B-3 proteinase-mediated cleavage, eliminated signalase cleavage at the 4A/4B site. In addition, the size of the 3(502)-4A product generated by trans processing of a truncated polyprotein, 3(502)-5(356), was consistent with cleavage at the 4A/2K site rather than at the downstream 4A/4B signalase site.
黄病毒蛋白是由宿主和病毒编码的蛋白酶对一个大的多聚蛋白进行共翻译和翻译后蛋白水解加工而产生的。由NS2B和NS3组成的病毒丝氨酸蛋白酶负责切割非结构区中至少四个双碱性位点(2A/2B、2B/3、3/4A和4B/5)。由于NS4B之前的氨基酸序列与用于将新生多肽转运到内质网腔中的信号肽具有共同特征,因此有人提出4A/4B位点的切割是由细胞信号肽酶介导的。在本报告中,利用无细胞翻译和体内瞬时表达试验研究黄热病毒多聚蛋白NS4区域的加工过程。用一个构建体,其包含由构成假定信号肽(sig4B)的17个残基之前的NS4B,在体外证明了在4A/4B位点的膜依赖性切割。令人惊讶的是,在无细胞翻译研究中未观察到NS4A-4B的加工,并且几种黄热病毒多聚蛋白的体内表达表明4A/4B切割仅在NS2B和NS3的蛋白酶结构域共表达期间发生。对NS3蛋白酶结构域的突变衍生物的检查表明,4A/4B位点的切割与活性NS2B-3蛋白酶的表达相关。根据这些结果,我们提出了一个模型,其中产生NS4B N末端的信号肽酶切割需要NS2B-3蛋白酶在一个新位点(称为4A/2K位点)进行先于它的切割,该位点在黄病毒中保守且位于信号肽酶位点上游23个残基处。为支持该模型,4A/4B信号肽酶位点的突变并未消除NS4区域的加工。相反,设计用于阻断NS2B-3蛋白酶介导切割的4A/2K位点的取代消除了4A/4B位点的信号肽酶切割。此外,由截短的多聚蛋白3(502)-5(356)的反式加工产生的3(502)-4A产物的大小与在4A/2K位点而非下游的4A/4B信号肽酶位点的切割一致。