Falgout B, Chanock R, Lai C J
Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892.
J Virol. 1989 May;63(5):1852-60. doi: 10.1128/JVI.63.5.1852-1860.1989.
Expression of dengue virus gene products involves specific proteolytic cleavages of a precursor polyprotein. To study the flanking sequences required for expression of the dengue virus nonstructural glycoprotein NS1, we constructed a series of recombinant vaccinia viruses that contain the coding sequence for NS1 in combination with various lengths of upstream and downstream sequences. The NS1 products expressed by these viruses in infected CV-1 cells were immune precipitated and analyzed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. The data show that the 24-residue hydrophobic sequence preceding NS1 was necessary and sufficient for the production of glycosylated NS1 and that this sequence was cleaved from NS1 in the absence of most dengue virus proteins. This finding is consistent with previous proposals that this hydrophobic sequence serves as an N-terminal signal sequence that is cleaved by signal peptidase. The cleavage between the C terminus of NS1 and the downstream protein NS2a occurred when the complete NS2a was present. Recombinant viruses containing NS1 plus 15 or 49% of NS2a produced proteins larger than authentic NS1, indicating that the cleavage between NS1 and NS2a had not occurred. Failure of cleavage was not corrected by coinfection with a recombinant virus capable of cleavage. These results suggest that NS2a may be a cis-acting protease that cleaves itself from NS1, or NS2a may provide sequences for recognition by a specific cellular protease that cleaves at the NS1-NS2a junction.
登革病毒基因产物的表达涉及前体多聚蛋白的特定蛋白水解切割。为了研究登革病毒非结构糖蛋白NS1表达所需的侧翼序列,我们构建了一系列重组痘苗病毒,这些病毒包含NS1的编码序列以及不同长度的上游和下游序列。这些病毒在感染的CV-1细胞中表达的NS1产物经免疫沉淀后,通过十二烷基硫酸钠-聚丙烯酰胺凝胶电泳进行分析。数据表明,NS1之前的24个残基疏水序列对于糖基化NS1的产生是必需且足够的,并且该序列在大多数登革病毒蛋白不存在的情况下从NS1上被切割下来。这一发现与之前的提议一致,即该疏水序列作为一个被信号肽酶切割的N端信号序列。当完整的NS2a存在时,NS1的C末端与下游蛋白NS2a之间会发生切割。含有NS1加上15%或49%的NS2a的重组病毒产生的蛋白比天然NS1大,这表明NS1与NS2a之间未发生切割。与能够切割的重组病毒共感染并不能纠正切割失败的情况。这些结果表明,NS2a可能是一种顺式作用蛋白酶,可从NS1上自我切割下来,或者NS2a可能提供序列以供特定细胞蛋白酶识别,该蛋白酶在NS1-NS2a连接处进行切割。